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HISTOPATHOLOGICAL STUDY OF SKIN TUMOURS
by
Dr. SONAM S. SHAIKH
Dissertation Submitted to the Rajiv Gandhi University Of Health Sciences, Karnataka, Bangalore
In partial fulfillment
of the requirements for the degree of
M.D.
in
PATHOLOGY
Under the guidance of
Dr. REKHA B. PURANIK M.D.,D.C.P. Professor,
Department of Pathology, Karnataka Institute of Medical Sciences,
HUBLI 2011
ii
DECLARATION BY THE CANDIDATE
I hereby declare that this dissertation/thesis entitled “Histopathological study
of skin tumours" is a bonafide and genuine research work carried out by me
under the guidance of Dr. Rekha B. Puranik, M.D.,D.C.P., Professor , Department of
Pathology, KIMS, HUBLI.
Date :
Place: Hubli
Dr. Sonam S. Shaikh, Post Graduate Student,
Department of Pathology, Karnataka Institute of Medical
Sciences, Hubli.
iii
Karnataka Institute of Medical Sciences, Hubli.
CERTIFICATE BY THE GUIDE
This is to certify that the dissertation entitled “Histopathological study of skin
tumours" is a bonafide research work done by Dr. Sonam S. Shaikh in partial
fulfillment of the requirement for the degree of M.D. Pathology.
Dr. Rekha B. Puranik, M.D.,D.C.P.,
Professor,
Department of Pathology,
Karnataka Institute of Medical
Sciences,
Hubli.
Date :
Place: Hubli
iv
Karnataka Institute of Medical Sciences, Hubli.
ENDORSEMENT BY THE HOD, PRINCIPAL/HEAD OF THE INSTITUTION
This is to certify that the dissertation entitled “Histopathological study of skin
tumours " is a bonafide research work done by Dr. Sonam S. Shaikh under the
guidance of Dr. Rekha B. Puranik, M.D.,D.C.P., Professor , Department of Pathology,
KIMS, Hubli.
.
.
Dr. U.S.Hangaraga M.D. Principal, KIMS, Hubli. Date: Place: Hubli.
Dr. Sujata S. Giriyan, M.D. Professor and Head, Department of Pathology, KIMS, Hubli. Date: Place: Hubli.
v
COPYRIGHT
Declaration by the Candidate
I hereby declare that the Rajiv Gandhi University of Health Sciences, Karnataka shall
have the rights to preserve, use and disseminate this dissertation / thesis in print or
electronic format for academic / research purpose.
© Rajiv Gandhi University of Health Sciences, Karnataka
Dr. Sonam S. Shaikh, Post Graduate Student,
Department of Pathology, Karnataka Institute of Medical
Sciences, Hubli.
Date : Place: Hubli
vi
ACKNOWLEDGMENT
It is most appropriate to begin by expressing my gratitude to the Almighty for
all His blessings.
I express my deep sense of gratitude and humble regards to my beloved
teacher and guide Dr. Rekha B Puranik,M.D, D.C.P Professor, Department of
Pathology, Karnataka Institute Of Medical College, Hubli, for her timely guidance,
suggestions and constant inspiration that enabled me to complete this dissertation.
I express my deep sense of gratitude to Dr. Sujata S. Giriyan, M.D, Professor
and Head, Department of Pathology, KIMS, Hubli for her expert guidance
,encouragement and advice.
I express my sincere thanks to my respected teachers Dr. M.H. Kulkarni M.D.,
Professor and Dr. P.K. Rangappa, M.D.,Professor for their guidance.
I am thankful to my teachers Dr. Sunitha Vernekar, Dr. Purushotham
Reddy, Dr. N.S.Kamkeri, Dr. Sateesh Chavan, Dr.Rajesh Chandan, Dr. Parvati
J, Dr. S.M.Choukimath, Dr. Rukmini S, Dr.Kavitha Y, Dr.Gulnaz Bendigeri,
Dr.Anil Kumar, Dr.Vidya M, Dr. Bharati, Dr. Malini, Dr.Arathi and Dr. Seemen
of Department of Pathology for their valuable support.
I owe my humble thanks to all the technical staff of Pathology for their
regular and timely help.
I express my sincere thanks to my post-graduate colleagues for their help and
kind cooperation in completing the study.
My sincere thanks to Dr. M.G.Hiremath, Director, KIMS and Dr. U.S.
Hangaraga, Principal, KIMS, Hubli for permitting me to carry out the study and use
the facilities in this Institution.
vii
I consider it my privilege to express my heartful thanks to my mother, Mrs
Manjit Shaikh, sister, brother, parents-in-law and friends for their inspiration,
goodwill and support given to me.
Above all I thank my husband, Shameer for the immense support, inspiration
and everlasting love.
Lastly I express my sincere thanks to all my patients for their contribution to
this study.
Dr. Sonam S. Shaikh, Post Graduate Student,
Department of Pathology, Karnataka Institute of Medical Sciences,
Hubli.
Date : Place: Hubli.
viii
LIST OF ABBREVATIONS USED
ALM - Acral Lentiginous Melanoma
BCC - Basal Cell Carcinoma
BD – Bowen Disease
Fig - Figure
LMM - Lentigo Maligna Melanoma
MM - Malignant Melanoma
NMSC- Non-Melanotic Skin Cancer
RGP -Radial Growth Phase
SCC- Squamous Cell Carcinoma
SSM - Superficial Spreading Melanoma
URGP -Unclassified radial growth phase
VGP- Vertical Growth Phase
WHO – World Health Organisation
ix
ABSTRACT
Background: Skin tumors constitute a small, but significant proportion of patients
with cancer. Skin tumors are an ideal subject for study from clinical and
morphological point of view and so ubiquitous that they affect people of all ages.
Objectives:
1. To find out the incidence of different tumors of skin .
2. To classify and identify various skin tumors and study their variations
according to age, sex and site.
3. To study the histomorphology of different skin tumors with ancillary
techniques wherever necessary.
Methodology: Biopsies and specimens received at the department of Pathology,
KIMS, Hubli from July 2005 to June 2010 were subjected to routine fixation,
processing and sectioning.
Results: Out of 218 cases presenting as skin tumors, 82 happened to be cysts and 1
pseudoepitheliomatous hyperplasia and out of remaining 135 tumors, 89(66%) were
malignant and 46(34%) benign. Squamous cell carcinoma formed the majority,
constituting 49 cases (55%) of all malignant tumors. Remainder comprised 20 cases
(22.5%) of BCC, 8 (9%) of verrucous carcinoma ,6 (6.7%) of malignant melanoma
and 6 (6.8%) of malignant adnexal tumors. Most common age group affected was 60-
69 yr in SCC ,malignant melanoma and adnexal carcinomas ,70-79yr in BCC; males
predominating SCC, BCC and MM. Most common site was face in BCC, foot in MM
and penis in SCC
x
Amongst the benign tumors, 10 (22%) were nevocellular nevus, 7(15%)
pilar tumor, 6(13%) each of verruca vulgaris and hidradenoma, 5(11%) seborrhoeic
keratosis, 4(9%) pilomatricoma, 2(5%) trichoepithelioma and 1(2%) case each of
syringoma, chondroid syringoma, cylindroma, apocrine hidrocystoma,
syringocystadenoma papilliferum and sebaceoma.
Conclusion: Histopathology is the most valuable means of diagnosis of skin tumours.
The diagnosis of skin tumors presents unique difficulties due to their wide variety,
overlapping differentiation and complicated nomenclature.
Key words: Squamous cell carcinoma, malignant melanoma, basal cell carcinoma.
xi
TABLE OF CONTENTS
Sl.No. Particulars Page No. 1. Introduction 1
2. Objectives 3 3. Review of Literature 4 4. Methodology 62 5. Results 64 6. Discussion 100 7. Conclusion 119 8. Summary 120 9. Bibliography 123 10. Annexures
a. Proforma 131
b. Key to master chart 137
c. Master chart 147
xii
LIST OF TABLES
Sl.No Tables Pages
1. Incidence of skin cancer 64
2. Distribution and incidence of benign and malignant tumours of 65
skin
3. Age incidence of benign tumours of skin 65
4. Age incidence of malignant tumours of skin 66
5. Sex incidence of benign and malignant tumours of skin 67
6. Incidence of different benign tumours of skin 68
7. Incidence of different malignant tumours of skin 70
8. Location of SCC in comparison with males and females 72
9. Age and sex incidence of squamous cell carcinoma 73
10. Conventional grading of squamous cell carcinoma 75
11. Broder’s grading of squamous cell carcinoma 75
12. Sex incidence of verrucous carcinoma 76
13. Location of verrucous carcinoma 76
14. Sex incidence of basal cell carcinoma 77
15. Location of basal cell carcinoma 77
16. Histological types of basal cell carcinoma 78
17. Sex incidence of malignant melanoma 80
18. Location of malignant melanoma 80
19. Clark’s grading of malignant melanoma 80
20. Incidence of skin appendageal tumours 82
21. Incidence of benign hair follicle tumours 83
xiii
22. Incidence of benign sweat gland tumours 85
23. Incidence of different adnexal carcinomas 87
24. Incidence of malignant neoplasms of skin in hospital 101
based Indian studies with respect to all malignant neoplasms
25. Comparative incidence of different malignant tumours of 102
skin in India
26. Comparison of sex distribution in squamous cell carcinoma 104
27. Comparison of site distribution in squamous cell carcinoma 104
28. Comparison of incidence of basal cell carcinoma with respect 105
to malignancies of skin
29. Comparison of histological types in basal cell carcinoma 106
30. Comparison of incidence of adnexal tumours 107
31. Comparison of incidence of benign appendageal skin tumours 107
32. Comparison of incidence of benign hair follicle tumours 108
33. Comparison of incidence of benign tumours of sweat gland 110
34. Comparison of incidence of different adnexal carcinoma 113
35. Comparison of incidence of malignant melanoma 115
36. Comparison of sex incidence of malignant melanoma 116
37. Comparison of age incidence of malignant melanoma 116
38. Comparison of site distribution of malignant melanoma 117
39. Comparison of location of malignant melanoma over foot 117
40. Comparison of clark’s grading of malignant melanoma 118
xiv
LIST OF FIGURES Sl.No Figures Pages
1. Parts of hair follicle 9
2. Sebaceous glands 12
3. Eccrine unit 12
4. Eccrine gland - secretory and duct portion 12
5. Apocrine gland 12
6. Incidence of benign and malignant tumours of skin 64
7. Sex incidence of benign and malignant tumours of skin 67
8. Site distribution of malignant tumors of skin 71
9. Location of squamous cell carcinoma in males and females 73
10. Age incidence of squamous cell carcinoma 74
11. Sex incidence of squamous cell carcinoma 74
12. Location & number of cases of basal cell carcinoma in head and neck 78
13. Histological types of basal cell carcinoma 79
14. Incidence of benign and malignant skin adnexal tumours 83
15. Squamous cell carcinoma of foot 89
16. Adenoid basal cell carcinoma 89
17. Malignant melanoma with inguinal lymph node metastasis 89
18. Verruca vulgaris 90
19. Pilomatricoma 90
20. Proliferating trichilemmal cyst 90
21. Hidradenocarcinoma 91
xv
22. Apocrine carcinoma 91
23. Seborrhoeic keratosis (40x, H&E) 92
24. Verrucous carcinoma (100x,H&E) 92 25. Cylindroma (100x, H&E), Inset (100x, PAS) 93 26. Apocrine hidrocystoma with squamous cell carcinoma (100x, H&E) 93 27. Hidradenoma (100x, H&E), Inset (400x,PAS) 94 28. Syringocystadenoma papilliferum (40x, H&E) 94 29. Chondroid Syringoma (100x, H&E) 95 30. Trichoepithelioma (100x, H&E) 95 31. Pilomatricoma (40x, H&E) 96 32. Proliferating trichilemmal tumour (100x, H&E) 96 33. Sebaceoma with extensive keratinisation (100x, H&E) 97 34. Malignant proliferating trichilemmal tumour (100x, H&E) 97 35. Hidradenocarcinoma (100x, H&E) 98
36. Malignant melanoma (400x, H&E) 98 37. Sebaceous carcinoma (100x, H&E) 99
1
INTRODUCTION
Little more than 100 years ago, the noted pathologist Rudolph Virchow
understood the skin as a protective covering for more delicate and functionally
sophisticated internal viscera.The skin is a complex organ.1 Because of its complexity
a wide range of diseases can develop from the skin including tumors from surface
epidermis, epidermal appendages and dermal tissue.
There has been an alarming increase of skin cancer among fair skinned
populations. Differences in trends and rates of skin cancer may be due to variation in
skin types, geographical latitudes, occupational exposure, behaviour in terms of sun
exposure and skin protection and differences in disease awareness and surveillance.2
Keratinocytic tumours account for approximately 90% of all skin malignancies
of which approximately 70% are basal cell carcinoma3. Melanocytic lesions are
important primarily because of malignant melanoma which is the single most
common potentially lethal neoplasm of skin4.There are a number of intraepidermal
proliferative disorders that may be precursors of squamous cell carcinoma3.
Cutaneous appendages give rise to a bewildering number of neoplasms, more
than accounted5. Adnexal tumours are rare and there is paucity of literature on their
clinicopathological features6. Benign adnexal tumours have a tendency to mimic
malignant lesion and usually manifest in older age group.6
2
The diagnosis of adnexal neoplasms presents unique difficulties, in part, related
to the wide variety of tumors, the substantial frequency of one lesion exhibiting
histologic features of two or more adnexal lines and the complicated nomenclature. 7
The distinction between benign and malignant neoplasm is rather more difficult
to define when they occur in skin and histopathological study is required to establish
diagnosis which is the most valuable means of diagnosis in dermatopathology inspite
of its own limitations.
The study of skin tumours is interesting, more intriguing, fascinating and
challenging because of its wide variations and there has been no systemic study being
done earlier.
Keeping in view these facts, an attempt is made to study the different varieties
of tumours of skin which will bear impact on patient management and prognosis.
3
AIMS AND OBJECTIVES
1. To find out the incidence of different tumours of skin.
2. To classify and identify various skin tumours and study their variations
according to age, sex and site.
3. To study the histomorphology of different skin tumors with ancillary
techniques wherever necessary.
4
REVIEW OF LITERATURE
HISTORY:
Percival Pott is the one first name that one associates with SCC who first
described it in 1775.8,9
The first description of BCC was by Jacob in 1827.8
Keratoacanthoma was first described by Sir Jonathan Hutchinson as a
‘crateriform ulcer of the face’ in 1889 and later clear cut morphological and biologic
behaviour was described by Mac Cormac and Scraff in 1936.10
The clinicopathological concept of verrucous carcinoma originated in 1948,
when Lauren V. Ackerman described it.11
The Spitz nevus was named after Sophie Spitz, who first described it in
1948.4,12
History of adnexal tumours
Pilomatricoma was first described in 1880 by Malherbe as a calcifying tumour
believed to arise from the sebaceous gland.13,14
The first report of ocular sebaceous carcinoma, in 1891, is credited to Allaire
although earlier cases were described by Malherbe and Robin and by Thiersch in
1865.15
Nasse in 1892 described the first case of mixed cutaneous tumour .16
Eccrine hidrocystoma was first described by Andrew Ross Robinson in
1893.17
Eccrine poroma was first described by Hermann Pinkus et al in 1956.18
Trichilemmoma was first designated as a neoplasm of outer root sheath by
Headington and French in 1962.19,20
In 1980, Lopansri and Mihm designated the term pilomatrix carcinoma.13
5
Embryology of skin
All constituents of skin are derived from either ectoderm or mesoderm. The
epithelial structures, that is, epidermis, folliculosebaceous-apocrine units, eccrine
units and nail units are derived from ectoderm. The other elements in skin, that is,
Langerhans’ cells, macrophages, blood and lymph vessels, muscles and adipocytes
originate from mesoderm. Melanocytes develop from neuroectoderm.21
Epidermis: The epidermis is derived from surface ectoderm. This is at first single
layered. By proliferation it gives rise to typical stratified squamous epithelium.22
Melanocytes are derived from neural crest cells in craniocaudal direction .23
Langerhans’cells are derived from bone marrow and Merkel cells from precursors of
epithelial cells of early fetal epidermis.23
Dermis: It is formed by condensation and differentiation of mesenchyme underlying
the surface ectoderm. The mesenchyme is believed to be derived from the dermatome
of the somites.22
Hair Follicle: Hair germs, or primary epithelial germs, in their earliest stage of
development consist of an area of crowding of deeply basophilic cells in the basal cell
layer of the epidermis. Subsequently, the areas of crowding develop into buds that
protrude into the dermis. Beneath each bud lies a group of mesenchymal cells from
which the dermal hair papilla is later formed.23
Sebaceous gland: Sebaceous gland develops from middle bulge of ectodermal cells
of hair follicle.23
Apocrine glands: Apocrine glands develop only in certain areas. Wherever they
form, they develop from the upper bulge of hair follicles that are in the early bulbous
peg stage.23
6
Eccrine glands: The eccrine gland germs begin as areas of crowding of deeply
basophilic cells in the basal layer of the epidermis.23 The downgrowth is first solid but
later it is canalised. The lower end of downgrowth becomes coiled and forms the
secretory part of the gland.22
Anatomical aspects of skin
The skin is the largest organ in the body, both in weight and surface area.24
The skin provides mechanical protection to underlying tissues. In this connection it is
thickest over areas exposed to greatest friction.25 The skin shows marked variations in
structure at different sites in the body surface.24
The epidermis is the thinnest component of skin, varying in thickness from about
0.04mm on the eyelids to 1.6mm on the palms of young adult; the average thickness
of epidermis is 0.1mm.The dermis is 15-40 times thicker than the epidermis.21
The surface of epidermis is marked by elevations and depressions. The
color of the skin is influenced by the amount of melanin present in the skin.25
Hairs are present on the skin covering almost the whole body. The sites
where they are not present include palms, soles, ventral surface and sides of digits and
some parts of genetalia.25 Hair is different morphologically and biologically on
different parts of the body.The different types of hair include lanugo, vellus and
terminal hairs.
At the body openings, skin is continuous with mucous membranes from
which it differs histologically by possessing a cornified layer of cells that lack
nuclei.21
7
Histology of skin
Understanding of the normal histology of skin is central to recognising
cutaneous pathology. The histology of the skin is amazingly complex. Divided into
two seemingly separate but functionally interdependent layers, epidermis and
dermis.23
Epidermis: The epidermal layer is composed primarily of keratinocytes (>90%), with
minority populations of Langerhans cells, melanocytes and neuroendocrine (Merkel)
cells.
The epidermis consists of stratified squamous epithelium in which following
layers can be recognised:
1. Basal cell layer (stratum basalis): The basal cells form a single layer, are columnar,
and lie with their long axis perpendicular to the dividing line between the epidermis
and the dermis. They have a basophilic cytoplasm often contain melanin pigment
transferred from adjacent melanocytes and contain a dark-staining oval or elongated
nucleus.23
2. Stratum spinosum (Malpighian layer): The polyhedral cells of the stratum spinosum
overlying the basal cell layer form a mosaic usually five to ten layers thick. The cells
are separated by spaces that are traversed by intercellular bridges.23 The cells appear
to have a number of spines hence they are also called prickle cells.25
3. Stratum granulosum: The cells of the granular cell layer are flattened and their
cytoplasm is filled with keratohyaline granules that are deeply basophilic and
irregular in size and shape.23
4. Stratum lucidum: This layer is so called because it appears homogeneous , the cell
boundaries being indistinct. It is well formed only in thick non hairy skin.25
8
5. Stratum corneum (Keratin layer): It is the outermost portion of epidermis and is
composed of a layer of flat, anuclear, eosinophilic corneocytes. Each elongated wafer-
like corneocyte covers an area occupied about 25 basal keratinocytes.21
Melanocytes: Melanocytes are melanin synthesizing dendritic cells located within the
basal layer of epidermis, hair bulb and outer root sheath of hair follicle. They contain
a small, dark-staining nucleus and largely as the result of shrinkage, a clear
cytoplasm. About 10% of the cells in the basal layer are melanocytes.23
Langerhans’ cells : Langerhans’ cells are named after Paul Langerhans,a medical
student who first described them in 1868.21These are bone-marrow-derived ,
dendritic, antigen presenting cells which appear as clear cells in the suprabasal
epidermis. Langerhans cells constitute 2% to 4% of the total epidermal cell
population.23
Merkel cells: Merkel cells are named after Friedrich Merkel who first described them
in 1875.21They are intraepidermal touch receptors present within the basal cell layer
of epidermis.24
Dermis:
The dermis is composed of bundles of collagen fibres and strands of elastic fibres
embedded in scanty amounts of acellular ground substance, together with occasional
inactive fibroblasts which synthesise the collagen, elastic fibres and matrix. The
dermis contains the vascular supply and innervation of the skin, and has two layers, a
superficial papillary dermis beneath the epidermis and a deeper reticular dermis which
borders the subcutis.
In addition there are skin appendages consisting of specialised structures such as
hair follicles, sweat glands and sebaceous glands.24
Hair: The hair follicle, with its hair in longitudinal sections, consists of three parts:23
9
A) The lower portion, extending from the base of the follicle to the insertion of
the arrector pili muscle.
B) The middle portion, or isthmus, extending from the insertion of the arrector
pili to the entrance of the sebaceous duct.
C) The upper portion, or infundibulum, extending from the entrance of the
sebaceous duct to the follicular orifice.
Fig1: Parts of hair follicle
A) The lower portion of the hair follicle is composed of five major portions:
I. The dermal hair papilla: It is formed of connective tissue in the shape
of inverted pine cone.21
II. The hair matrix: The pluripotential cells of the hair matrix present in
the hair bulb give rise to the hair and to the inner root sheath. The cells
of the hair matrix have large vesicular nuclei and a deeply basophilic
cytoplasm.23
Lower segment
10
III. The hair consists, inward to outward of medulla, cortex, and hair
cuticle. The hair cortex consists of cells that keratinize gradually
without the formation of keratohyaline granules representing hard
keratin. The hair cuticle cells are arranged like shingles , tightly
interlocked with the cells of the inner root sheath cuticle.23
IV. Inner root sheath, consisting inward to outward of inner root sheath
cuticle, Huxley layer, and Henle layer. None of these three layers
contains melanin. All three layers keratinize by means of trichohyalin
granules.23
V. Outer root sheath: The outer root sheath extends upward from the
matrix cells at the lower end of the hair bulb to the entrance of the
sebaceous duct, where it changes into surface epidermis, which lines
the infundibulum of the hair follicle. The outer root sheath cells have a
clear, vacuolated cytoplasm because of the presence of considerable
amounts of glycogen.23
B. The isthmus: Here the outer root sheath is no longer covered by the inner root
sheath, which by then has keratinized and disintegrated. The outer root sheath
therefore undergoes trichilemmal keratinisation
C. Infundibulum: It is lined by surface epidermis, which undergoes epidermal
keratinisation.23
Sebaceous glands: A sebaceous gland may consist of one or several lobules leading
into a common excretory duct composed of stratified squamous epithelium opening
into hair follicle.21,23 Sebaceous glands, being holocrine glands, form their sebum by
decomposition of their cells.23,24 Each sebaceous lobule possesses a peripheral layer of
cuboidal, deeply basophilic cells that usually contain no lipid droplets. The more
11
centrally located cells are mature with central nucleus and foamy cytoplasm and
contain lipid droplets (Fig.No.2).23
Eccrine glands: Eccrine glands are present everywhere in the human skin and are
found in greatest abundance on the palms and soles and in the axillae. Eccrine glands
are composed of three segments: intraepidermal duct, intradermal duct, and secretory
portion (Fig.No.3).
The secretory portion of the eccrine gland makes the basal coil composed of
a distinct layer of secretory cells and the outer layer of myoepithelial cells with a
peripheral hyaline basement membrane zone. The secretory cells lining the lumen
consist equally of two types, clear cells and dark cells (Fig 4).
The intradermal eccrine duct is composed of two layers of small, cuboidal,
deeply basophilic epithelial cells with lumen lined by eosinophilic cuticle.
The intraepidermal eccrine duct or acrosyringium extends from the base of a
rete ridge to the surface and follows a spiral course, consisting of a single layer of
inner or luminal cells and two or three rows of outer cells.23
Apocrine glands: Apocrine glands are encountered in only a few areas: in the axillae,
in the anogenital region, and as modified glands in the external ear canal (ceruminous
glands), in the eyelid (Moll's glands), and in the breast (mammary glands).
Apocrine glands are composed of the duct portion and the secretory portion.
The duct of an apocrine gland usually leads to a pilosebaceous follicle showing a
double layer of basophilic cells and a periluminal eosinophilic cuticle. The secretory
portion of the apocrine gland shows a single layer of secretory cells and an outer layer
of of myoepithelial cells.23 The glandular cells show apocrine secretion which gives
the appearance of being decapitated or pinched off (Fig No.5).21
12
Fig 2:Sebaceous gland Fig 3: Eccrine unit
Fig 4: Eccrine gland - secretory and duct Fig 5: Apocrine gland
13
WHO histological classification of skin tumours3
1) Keratinocytic tumours
Malignant
Basal cell carcinoma
Superficial basal cell carcinoma
Nodular (solid) basal cell carcinoma
Micronodular basal cell carcinoma
Infiltrating basal cell carcinoma
Fibroepithelial basal cell carcinoma
Basal cell carcinoma with adnexal differentiation
Basosquamous carcinoma
Keratotic basal cell carcinoma
Others
Squamous cell carcinoma
Acantholytic squamous cell carcinoma
Spindle-cell squamous cell carcinoma
Verrucous squamous cell carcinoma
Pseudovascular squamous cell carcinoma
Adenosquamous carcinoma
Benign
Bowen disease
Bowenoid papulosis
Actinic keratosis
Arsenical keratosis
PUVA keratosis
Verrucas
Verruca vulgaris
Verruca plantaris
Verruca plana
Acanthomas
Epidermolytic acanthoma
Warty dyskeratoma
Acantholytic acanthoma
14
Lentigo simplex
Seborrhoeic keratosis
Melanoacanthoma
Clear cell acanthoma
Large cell acanthoma
Keratoacanthoma
Lichen planus-like keratosis
2) Melanocytic tumours
Malignant melanoma:
Superficial spreading melanoma
Nodular melanoma
Lentigo maligna
Acral-lentiginous melanoma
Desmoplastic melanoma and desmoplastic neurotropic melanoma
Melanoma arising from blue naevus
Melanoma arising in giant congenital naevi
Childhood melanoma
Naevoid melanoma
Persistent melanoma and local metastasis of melanoma
Benign
Congenital melanocytic naevus
Superficial type
Proliferative nodules in congenital melanocytic naevi
Blue naevi
Cellular blue naevus
Dermal melanocytic lesions
Mongolian spot
Naevus of Ito and naevus of Ota
Combined naevus
Melanotic macules
Simple lentigo – lentiginous melanocytic naevus
Dysplastic naevus
Site specific naevi
Acral naevus
15
Genital naevus
Meyerson naevus
Persistent (recurrent) melanocytic naevus
Spitz naevus
Pigmented spindle cell naevus (Reed)
Halo naevus
3) Classification of appendageal tumors
Tumours with apocrine and eccrine differentiation:
Malignant tumours:
Tubular carcinoma
Microcystic adnexal carcinoma
Porocarcinoma
Spiradenocarcinoma
Malignant mixed tumour
Hidradenocarcinoma
Mucinous carcinoma
Digital papillary carcinoma
Adenoid cystic carcinoma
Apocrine carcinoma
Paget disease of breast
Extramammary Paget disease
Benign tumours
Hidrocystoma
Syringoma
Poroma
Syringofibroadenoma
Hidradenoma
Spiradenoma
Cylindroma
Tubular adenoma
Tubular papillary adenoma
Syringocystadenoma papilliferum
Hidradenoma papilliferum
Mixed tumour (chondroid syringoma)
16
Tumours with follicular differentiation
Malignant tumours
Pilomatrical carcinoma
Proliferating trichilemmal tumour
Benign tumours
Trichoblastoma
Pilomatricoma
Tricholemmoma
Multiple tricholemmomas
Trichofolliculoma
Fibrofolliculoma / trichodiscoma
Tumours with sebaceous differentiation
Sebaceous carcinoma
Sebaceous adenoma
Sebaceoma
Cystic sebaceous tumour
Cysts are classified as follows26:
Follicular cysts
Infundibular cyst
Trichilemmal cyst
Steatocystoma multiplex
Dermoid cyst
Eruptive vellus hair cyst
Milia
Bronchogenic and thyroglossal duct cysts
Cutaneous ciliated cyst
Median raphe cyst of the penis
17
Squamous cell carcinoma (SCC)
Squamous cell carcinoma is a malignant neoplasm of epidermal keratinocytes
in which the component cells show variable squamous differentation.3 Various reports
from India have consistently reported SCC as the most prevalent skin cancer.27
Clinical features: squamous cell carcinoma of the skin most commonly consists of a
shallow ulcer surrounded by a wide, elevated, indurated border.26 Cutaneous SCC is
more in men than in women, in older age groups and in those with fair skin.28
Squamous cancers could be divided into the ones which arise de-novo, that is
without pre-existing lesion and the other induced type, that is definite association of
the cancer with predisposing local cause.29,30 Marjolin in 1828 suggested the origin of
skin cancer in burns and hence the name Marjolins ulcer came into being from his initial
description.29 Chakravorthy and Dutta-Choudhuri in 1968 encountered SCC developing
with chronic infection of the interdigital webs and gave the name web cancer.29
The carcinomatous change in the loin due to constant irritation produced by dhoti is
called ‘Dhoti cancer’.29 described by Khanolkar and Suryabhai in 1945.27
Histopathology: SCC consists of irregular masses of epidermal cells that proliferate
downward into the dermis. The invading tumor masses are composed in varying
proportions of normal squamous cells and of atypical (anaplastic) squamous cells.
Differentiation in squamous cell carcinoma is in the direction of keratinisation which
takes place in the form of horn pearls composed of concentric layers of squamous cells
showing gradually increasing keratinization toward the center.26
In 1932 Broder introduced a formal grading system based on keratinocyte
differentiation that is still used today. Tumours are graded from one to four grades
based on increasing percentage of undifferentiated cells.9,28
Grade 1: More than 75% cells are differentiated, many horn pearls are seen.
18
Grade 2: More than 50% cells are differentiated, keratinisation is less prominent.
Grade 3: More than 25% cells are differentiated, cells are atypical.
Grade 4: Less than 25% cells are differentiated, keratinisation is absent.
SCC are conveniently classified into well differentiated , moderately differentiated and
poorly differentiated.28
Well differentiated : Squamous cells show abundant keratinisation
Intercellular bridges are readily apparent
Minimal pleomorphism
Mitotic figures are basally located
Moderately differentiated : Squamous epithelial derivation is less obvious
Pleomorphism is more pronounced
Less keratin formation
Mitotic figures are more common
Poorly differentiated SCC: Atypicality of cells is higher26
Variants of SCC
Spindle cell SCC:
This is an uncommon poorly differentiated variant of squamous cell carcinoma that
exhibits a prominent spindle cell morphology.The spindle cells have a large vesicular
nucleus and scanty eosinophilic cytoplasm, often with indistinct cell borders. There is
variable pleomorphism, usually with many mitoses.3
Acantholytic SCC:
Synonyms: Adenoid SCC, Pseudoglandular SCC3
Acantholytic squamous cell carcinoma is a histologic variant of cutaneous
SCC that is histologically defined by loosening of the intercellular bridges resulting in
acantholysis.3
19
Verrucous carcinoma
Synonyms- Ackerman’s tumour, epithelioma cuniculatum, giant condyloma
acuminatum, Buschke-Lowenstein tumour, papillomatosis cutis carcinoides 3
The clinicopathological concept of verrucous carcinoma originated in 1948,
when Lauren V. Ackerman described it in oral cavity and called it as Ackerman’s
tumour . He used the term Verrucous carcinoma to denote this concept of a locally
aggressive ,exophytic ,low grade SCC of little metastatic potential.11
In 1954, Aird et al described the foot counterpart of the same tumour and coined
it as Epithelioma cuniculatum.11,31 The cuniculatum is Latin word for rabbit warren
reflecting this tumour’s many sinuses and keratin filled cysts . verrucous carcinoma can
occur anywhere on the skin and known by several different names .11,26
Verrucous carcinoma of the genitoanal region, also called giant condylomata
acuminatum of Buschke and Loewenstein, most commonly occurs on the glans penis
and foreskin of uncircumcised male and on other cutaneous sites it is called
papillomatosis cutis carcinoides.11,26
Histopathology
For the diagnosis of verrucous carcinoma, a large, deep biopsy is essential. The
superficial portions generally resemble a verruca by showing hyperkeratosis,
parakeratosis, and acanthosis. The keratinocytes appear well differentiated, stain lightly
with eosin, and possess a small nucleus. The tumor invades with broad strands that often
contain keratin-filled cysts in their center. There are large, bulbous, downward
proliferations that compress the collagen bundles and push them aside. Even in the
deep portions of the tumor, nuclear atypia, individual cell keratinization, and horn pearls
are absent.26
20
Basal Cell Carcinoma (BCC)
Syn: Basal cell epithelioma , trichoblastic carcinoma.3
The first description of BCC was by Jacob in 1827.8 BCC is the most common
malignant skin tumour but the incidence in Asian races is lower than the white race.32
The incidence of BCC in Indian literature ranges from 12% to 30%.33 BCC is seen
almost exclusively on hair bearing skin especially on face.26 BCC generally occurs in
adults.26 BCC may develop in children under following circumstances: Nevoid basal
cell epithelioma syndrome, in pre-existing organoid nevus and in xeroderma
pigmentosa.34 As a rule BCC do not metastasize.26
There are five clinical types of BCC which include 26,28,35
1. Nodulo-ulcerative
2. Pigmented
3. Morphea-like or fibrosing basal cell carcinoma
4. Superficial (multifocal)
5. Fibroepithelioma of Pinkus
Noduloulcerative (rodent ulcer) begins as a small, waxy nodule that often
undergoes central ulceration. A typical lesion then consists of a slowly enlarging ulcer
surrounded by a pearly, rolled border. Pigmented basal cell carcinoma differs from the
noduloulcerative type only by the brown pigmentation of the lesion.26
Scriverer Y et al in his study on 13,457 patients with BCC have shown that
nodular and morphoeiform types predominate on forehead where as trunk is the most
common site for superficial type.36
Histopathology: Basal cell carcinomas tend to share the common features of a
predominant basal cell type, peripheral palisading of lesional cell nuclei, a specialized
stroma, and clefting artifact between the epithelium and the stroma.
21
Basal cell carcinomas can be divided into two groups: undifferentiated and
differentiated. Those of the latter group show a slight degree of differentiation towards
the cutaneous appendages. Basal cell carcinomas showing no differentiation are called
solid basal cell carcinomas. They can be subdivided into circumscribed and infiltrative.
Solid Circumscribed: shows tumor masses of various sizes and shapes embedded in
the dermis. The peripheral cell layer of the tumor masses often shows a palisade
arrangement, whereas the nuclei of the cells inside lie in a haphazard fashion.26
Solid infiltrative : Reffered to as aggressive BCC by Jacob et al. 37Aggressiveness is a
mearurement of local spread indicated by poor circumscription and deep invasion into
muscle ,cartilage or bone .37 Cell aggregates display irregular configuration , little or no
palisading and perineural invasion.26
Keratotic BCC : shows differentiation towards hair structures show parakeratotic cells
in strands , whorls and horn cysts and undifferentiated cells , thus resembling
trichoepithelioma .26 Johnson and Bennet described four patients who developed BCC
among facial trichoepitheliomas .38
Adenoid basal cell carcinoma : shows formations suggesting tubular, gland-like
structures. The cells are arranged in intertwining strands and radially around islands of
connective tissue, resulting in a tumor with a lace-like pattern.
BCC with sebaceous differentiation shows essentially a basal cell carcinoma in which
there are interspersed aggregates of sebaceous cells and cells transitional from basaloma
cells to sebaceous cells.
Pigmented BCC: shows large amount of melanin in benign melanocytes that colonise
the tumour. Melanophages are seen in connective tissue stroma and even the tumour
cells may contain little melanin.
22
Superficial BCC : Superficial basal cell carcinoma shows buds and irregular
proliferations of tumor tissue attached to the undersurface of the epidermis.26
Micronodular BCC: In 1986, Lang and Maize coined the term ‘micronodular’ to
distinguish a histological subtype of BCC which was difficult to eradicate than nodular
BCC.39 It is characterised by basaloid cellular proliferation arranged in small nests.28
Peripheral palisading is less prominent and retraction artefact is absent.28,39
Morpheaform (sclerosing) BCC: Small cords and narrow strands of basaloid cells are
embedded in dense fibrocytic and desmoplastic stroma.28
Metatypical (Basosquamous) BCC:shows foci neoplastic squamous differentiation in
BCC. 28
Other rare histopathological varients include :
Adamantinoid basal cell carcinoma: shows a great histologic resemblance to
adamantinoma . One observes solid masses of basaloma cells with palisading at the
periphery. Inside this layer, the cells show elongated nuclei and stellate cytoplasm.
Granular basal cell carcinoma : some of the tumor cells have the usual appearance of
basaloma cells, whereas others show a gradual transition to granular cells which show in
their cytoplasm numerous eosinophilic granules .
Clear cell basal cell carcinoma: the clear cell pattern may occupy all or part of the
tumor islands. The clear cells contain vacuoles of different sizes filled with
glycogen.The vacuoles often cause peripheral displacement of the nucleus, giving the
cells a signet-ring appearance.26
Basal cell carcinoma with matricial differentiation : shows islands of shadow cells,
as seen in pilomatricoma, are located within a basal cell carcinoma.26
Keloidal BCC : thick keloidal collagen bundles are the main component of stroma.35
Fibroepithelioma of Pinkus: was first described in 1953 consists of long, thin,
23
branching, anastomosing strands of basal cell carcinoma are embedded in a fibrous
stroma. Many of the strands show connections with the surface epidermis.26
Bowen disease
Synonyms: Squamous cell carcinoma in situ, bowenoid dysplasia, bowenoid
squamous carcinoma in situ (BSCIS), vulvar intraepithelial neoplasia (VIN III).3
Bowen disease (BD) is a form of squamous cell carcinoma in situ.3 Clinically
lesions are single or multiple slowly enlarging persistant erythematous patch of
irregular outline with areas of scaling or crusting most commonly seen on head trukk,
extremities and genetalia.28These lesions occurring on the glans penis are referred to as
erythroplasia of Queyrat.26
Histologically, it shows hyperkeratosis, parakeratosis, acanthosis with
increased cellularity, and a chronic inflammatory infiltrate in the upper dermis. The
epidermis exhibits loss of normal polarity and normal surface keratinocytic maturation.
A “windblown” appearance of crowding of atypical keratinocytes, with
hyperchromatism, pale-staining to vacuolated cells, occasional multinucleated cells,
dyskeratosis, and abnormal mitoses are noted. These changes are confined by an intact
basement membrane.3
Actinic Keratosis:
Synonyms : Solar keratosis3, Senile keratosis28
Actinic keratosis is an intraepidermal neoplasm of sun-damaged skin
characterized by variable atypia of keratinocytes. Actinic keratoses usually present in
older individuals as circumscribed ,<1cm scaly macules or slightly elevated papules or
plaques, ranging from erythematous to grey-brown with adherent yellow-brown scale.3
24
Only a small proportion of actinic keratosis( 0.1-10%) develop into invasive
squamous cell carcinoma.28 Solar keratosis is a sensitive indicator of a person’s
exposure to sunlight over the years.40 Histologically six types are described.3
1. Hypertrophic type: shows pronounced hyperkeratosis usually intermingled with
areas of parakeratosis. Also shows acanthosis with the cells of stratum malpighii
showing a loss of polarity and thus a disorderly arrangement, pleomorphism and
anaplasia. Often the nuclei in the basal layer are closely crowded together.
2. Atrophic type: the epidermis is thinned and devoid of rete ridges. Atypicality of the
cells is found predominantly in the basal cell layer.26
3. Bowenoid type: involve full thickness epidermis and is difficult to differentiate
from Bowen disease.
4. Acantholytic type: shows suprabasal clefting, with varying acantholysis and
dyskeratosis.
5. Pigmented type: shows increased melanisation of atypical keratinocytes and dermal
melanophages.3
6. Lichenoid variant: shows nuclear atypia, irregular acanthosis and hyperkeratosis,
the presence of degeneration of the basal cell layer, and a bandlike lichenoid
infiltrate in close apposition to the epidermis including Civatte bodies.26
Verrucas3: Verrucas or condyloma are common, contagious, epithelial tumours caused
by human papillomaviruses (HPV).
Synonyms: Verruca vulgaris (common warts); verruca palmaris (deep palmar ); verruca
plantaris (deep foot warts); superficial plantar warts; verruca planae ( flat warts);
25
condylomata acuminata (genital warts).
Verruca vulgaris: Verruca vulgaris is a benign, squamous papillomatous lesion caused
by infection with the HPV.
Histologically show marked hyperkeratosis, acanthosis, papillomatosis,
parakeratosis, hypergranulosis, koilocytosis and inward turning of elongated rete ridges.
Dilated vessels are often found in the core of the papillomatous projections. Most warts
are only a cosmetic problem.
Verruca plantaris occurs on sole of foot and is characterised by the formation of
thick, hyperkeratotic lesions. Verruca plana are flat topped papules characterised by
loose hyperkeratosis with basket-weave-pattern but little or no papillomatosis as in
verruca vulgaris.
Seborrhoeic keratosis
Synonyms: Senile wart, basal cell papilloma41
Seborrheic keratosis are common,often multiple, benign tumours which
usually appear in middle age.41They are sharply demarcated gray-brown to black lesions
which are sharply raised with a stuck on appearance.26,41
Histologically, shows a sharply defined tumor which can be endophytic or
exophytic composed of basaloid cells with a varying admixture of squamoid cells.
Keratin filled invaginations and horn cysts are characteristic features.41
Six histologic types are described by Lever et al.
a. Acanthotic type (Solid type): Epidermis is greatly thickened with slight
hyperkeratosis and papillomatosis.Pseudo-horn cysts are numerous. The lower border of
the tumor is even and gradually lies on a straight line that may be drawn from normal
epidermis at one end of tumor to the other normal end. The amount of melanin is
26
usually more than normal.
b. Hyperkeratotic type: Hyperkeratosis and papillomatosis are pronounced, whereas
acanthosis is not very conspicuous.26
c. Reticulated Type (Adenoid Type): This has interlacing thin strands of basaloid
cells, often pigmented enclosing small horn cysts.41
d. Clonal type (Nesting): This shows intraepidermal nests of basaloid cells resembling
Borst-Jadassohn phenomenon.41
e. Irritated type: In the irritated type of seborrheic keratosis, squamous cells
outnumber basaloid cells. Numerous whorls or eddies resembling poorly differentiated
horn pearls are present and in addition, may show areas of downward proliferation
breaking through the horizontal demarcation .Inflammation is usually mild or absent.26
f. Melanoacanthoma: This is a rare variant of pigmented seborrheic keratosis. It is a
benign mixed tumour of melanocytes and keratinocytes. Many melanocytes scattered
throughout the tumor mass.26
Keratoacanthoma
Synonyms: Kyste Sebace atypique, self-healing primary SCC, tumor like keratosis.10
Keratoacanthoma is a relatively common, rapidly growing benign neoplasm
of the skin that may be self limited, but may cause local destruction. First described by
Sir Jonathan Hutchinson as a ‘crateriform ulcer of the face’ in 1889, clear cut
morphological and biologic behaviour was described by Mac Cormac and Scraff in
1936.10
Keratoacanthoma can be solitary, multiple or subungual.26 Solitary
keratoacanthoma occurs in 6th to 7th decades in sun exposed areas. There are three
stages of keratoacanthoma.10
27
1. Proliferative stage: shows a firm, hemispheric smooth enlarging papule.
2. Mature stage: Bud shaped, dome shaped or berry shaped skin coloured or
erythematous nodule with central, often umbilicated keratotic core.
3. Resolving stage: Appears as a keratotic, necrotic nodule which heals by leaving
slightly depressed hypopigmented scar.
Histologically the lesion shows
1. Proliferative phase: Horn filled invagination of epidermis from which epidermal
strands extend into the dermis. These epidermal strands may show nuclear atypia,
multiple mitotic figures including tripolar forms. Some tumor regions may show
pronounced keratinisation with abundant pale staining cytoplasm producing a
eosinophilic glassy appearance.
2. Mature stage: shows a keratin filled crater at the centre of epidermis which extends
like a lip over the sides of the crater. Keratinisation is extensive and microabscesses
may be evident with dense inflammatory infiltrates at the base of the lesion.
3. Involution/Resolving stage: The lesion becomes less crateriform and most cells at
the base of the crater are keratinised. A mixed dermal infiltrate with multinucleate giant
cells is seen. The crater slowly becomes flat and heals with formation of scar.10
Keratoacanthoma is considered to be an abortive malignancy which only rarely
progresses into an invasive carcinoma.44 It is well known that they can exhibit
perineural invasion.45
Warty Dyskeratoma:
Warty dyskeratomas are rare, usually solitary lesions seen in elderly.41The center
of the lesion is occupied by a large, cup-shaped invagination connected with the surface
by a channel filled with keratinous material. The large invagination contains numerous
acantholytic, dyskeratotic cells in its upper portion.26
28
Clear cell acanthoma:
First described in 1962. It is a rare, usually solitary red nodule, commonly seen
in the lower limbs.26 Histologically it shows a sharply demarcated area of epidermis in
which the cells are clear and slightly enlarged. These cells reveal presence of glycogen.
The basal layer is spared.26Other epidermal changes include mild spongiosis, exocytosis
of neutrophils which may form microabscess and parakeratosis.
Cysts :
Epidermal cyst
Epidermal cysts are slowly growing, elevated, round, firm, intradermal or subcutaneous
tumors that cease growing after having reached 1 to 5 cm in diameter. They occur most
commonly on the face, scalp, neck, and trunk.26 The term 'sebaceous cyst' has been used
to describe most, if not all, cystic lesions of the skin as the contents of these lesions
appear to be sebaceous on casual examination. Kligman in 1964 studied the so-called
sebaceous cysts and concluded that they were nothing more than a variety of keratinous
cyst.46
Histopathology: Epidermal cysts have a wall composed of true epidermis with a distinct
granular layer. The cyst is filled with horny material arranged in laminated layers. When
an epidermal cyst ruptures and the contents of the cyst are released into the dermis and
elicit a foreign-body reaction .26
Origin : Most spontaneously arising epidermal cysts are related to the follicular
infundibulum.26 Keratotic plugging (Auroroa and Blodi,1972) seems a reasonable
explanation in some of these cases, which obstruct the pilosebaceous canal.46
Pilar cyst:
Synonym: Trichilemmal cyst, trichochlamydo cyst47
Pilar cysts are less common than epidermal cysts and about 90% of trichilemmal cysts
29
occur on the scalp.26
Histopathology: The wall of trichilemmal cysts is composed of epithelial cells
possessing no clearly visible intercellular bridges. The basal or peripheral layer of cells
shows a distinct palisade arrangement. The epithelial cells close to the cystic cavity
appear swollen, with pale cytoplasm and generally undergo abrupt keratinisation
without a granular layer. The content of the cysts consists of homogeneous eosinophilic
material.26
Dermoid cyst:
Dermoid cysts are subcutaneous cysts that usually are present at birth. They occur most
commonly on the head, mainly around the eyes, and occasionally on the neck. When
located on the head, they often are adherent to the periosteum. Usually they measure
between 1 and 4 cm in diameter. Histopathologically dermoid cysts are lined by an
epidermis that possesses various epidermal appendages that are usually fully matured.26
Classification of Appendageal Tumors
Adnexal tumours of skin, though rare, have been recognised from later part
of 19th century. The first case of a mixed tumour of skin was reported by Nasse.48
Historically, tumors of the epidermal appendages have been classified into four groups
that exhibit histologic features analogous to hair follicles, sebaceous glands, apocrine
glands, and eccrine glands, according to a gradient of decreasing differentiation.7
Adnexal tumours may display more than one line of differentiation, rendering precise
classification more difficult.49
Various classifications have been proposed in the past, which have required
modification from time to time in the light of most recent ultrastructural and
histochemical findings and the reporting of new morphological entities.
30
Classification of tumors of epidermal appendages by Lever et al26
Follicular Differentiation
Sebaceous Differentiation
Apocrine Differentiation
Eccrine Differentiation
Hyperplasias, hamartomas
Hair follicle nevus Dilated pore Generalized hairfollicle hamartoma Basaloid follicular hamartoma
Nevus sebaceous Sebaceous hyperplasia
Apocrine nevus Eccrine nevus
Benign neoplasms
Trichofolliculoma Pilar sheath acanthoma Fibrofolliculoma Trichodiscoma Trichoepithelioma Trichoblastoma Trichoadenoma Pilomatricoma Trichilemmoma Tumor of follicular infundibulum Trichilemmal horn Proliferating trichilemmal cyst
Sebaceous adenoma Sebaceoma
Aprocrine hidrocystoma Hidroadenoma papilliferum Syringocystadenomapapilliferum Tubular apocrine adenoma Erosive adenomatosisof thenipple Apocrine cylindroma
Eccrine hidrocystoma Syringoma Eccrine cylindroma Eccrine poroma Eccrine syringofibroadenoma Mucinous syringometaplasia Eccrine spiroadenom Papillary eccrine adenoma Nodular hidradenoma Chondroid syringoma
Malignant neoplasms
Pilomatrix carcinoma Malignant proliferating trichilemmal tumor Trichilemmal carcinoma Trichoblastic carcinoma
Sebaceous carcinoma
Malignant apocrine cylindroma
Porocarcinoma Malignant eccrine spiroadenoma Malignant nodular hidradenoma Malignant chrondroid syringoma Eccrine adenocarcinoma Microcystic adnexal carcinoma Aggressive digital papillary adenocarcinoma Adenoid cystic carcinoma Mucinous eccrine carcinoma Syringoid eccrine carcinoma Malignant eccrine cylindroma
31
Histogenesis of adnexal tumours (Cell of origin)
Histogenesis is a concept that implies that the histologic appearance of a
tumor is similar to the histology of the organ/structure from which the tumor arose.7
Histochemical and electron microscopic investigations have been useful in
the determination of histogenesis of many appendage tumors. The immature cells of
appendage tumours, like immature cells of cutaneous appendages of human embryo,
contain certain enzymes that are specific for each cutaneous appendage. The electron
microscopic examination of the appendage tumours reveals details which are not
recognizable on examination with light microscope.50 The advent of
immunoperoxidase methods has “made the unknown a different colour,” yet the
results of so called brown stains have resolved few if any of the conundrums of
adnexal classification.18
Three possibilities exist for the development of appendageal tumors-
1. In 1948, the thesis was advanced that cutaneous tumors differentiating toward hair,
sebaceous glands, or apocrine glands developed from primary epithelial germ cells.
The hyperplasias, adenomas, and benign epitheliomas arose from primary epithelial
germ cells that had attained a certain degree of differentiation before the onset of
neoplasia.
2. The stem cells are continually present in the skin and it is likely that the
appendageal tumors arise from these cells. Appendageal tumors associated with
genetic syndromes, such as multiple cylindromas and multiple trichoepitheliomas are
32
probably derived from abnormally regulated pluripotent cells that are directed to form
abnormal appendageal structures rather than mature appendages.
3. Originate from cells of pre-existing structures.7
Tumors with hair follicular differentiation
Trichofolliculoma
Trichofolliculoma is a rare pilar tumour.5 It occurs in adults as a solitary lesion,
consists of a small, skin-colored, dome-shaped nodule. Frequently, there is a central
pore. If such a central pore is present, a wool-like tuft of immature, usually white
hairs may be seen emerging from it, a highly diagnostic clinical feature.
Histologically it consists of a large cystic space that is lined by squamous
epithelium and contains horny material and frequently fragments of birefringent hair
shafts.7 Numerous secondary and tertiary follicles surrounded by various number of
sebaceous glands bud out and branch radially from the central cavity into a fibrotic
stroma.49
Trichoblastoma
Trichoblastomas are extremely rare benign tumours of the hair germ .5They are upto
one cm in size and most commonly occur on scalp.7
Histoologically trichoblastomas consist of a proliferation of follicular germ
cells manifested by a combination of various proportions of mesenchymal and
epithelial cells. A spectrum of lesions is seen depending on the proportions of
mesenchymal and epithelial components. At one end is the predominantly
mesenchymal variant, termed the trichogenic fibroma, and at the other is classic
trichoblastoma with predominantly basaloid epithelial cells. These basaloid islands
33
demonstrate peripheral palisading and a fibrocellular stroma similar to that of
surrounding follicles with no overlying epidermal connection.7
Trichoadenoma5,7
It is a rare solitary tumor with hair follicle like differentiation and occurs as a nodule
over face or buttocks. Histologically shows well-defined dermal tumor consisting of
epithelial islands most of which have central cystic cavity lined by squamous
epithelium with epidermoid keratinisation and fibrous stroma. This tumour
differentiates towards the infundibular portion of the pilosebaceous unit.
Trichoepithelioma
Synonyms- Epithelioma adenoids cysticum of Brook,7,51 Multiple benign cystic
epithelioma.7
Trichoepitheliomas are benign cutaneous epithelial-mesenchymal
tumours best classified as poorly differentiated hamartomas of hair germ. They are
characteristically either multiple or solitary.47 There are three varients: solitary,
multiple and desmoplastic.5
Solitary trichoepitheliomas are found as skin coloured papules, with a
predilection for nose, upper lip and cheeks. Multiple lesions have autosomal dominant
mode of inheritance.5
Histologically it is a well circumscribed dermal lesion with or without focal
continuity with epidermis.5,49 It consists predominantly of uniform basaloid cells with
peripheral palisading arranged in nests , trabeculi and cribriform patterns surrounded
by dense fibroblastic stroma representing abortive attempts to form papillary
34
mesenchyme.5,49Formation of small keratinous cysts lined by flattened squamous cells
containing keratohyaline granules and showing an abrupt zone of keratinisation is
seen.47 Tatnall and Wilson Jones in 1988 have reported three cases of solitary giant
trichoepitheliomas occurring in perianal region.52
The histogenesis of trichoepithelioma is uncertain.47 An IHC analysis
suggests the differentiation of tumour towards outer root sheath.7 The close
relationship between trichoepithelioma and basal cell carcinoma has been explained
on the basis of the assumption that they have a common genesis from pluripotential
cells, which, like primary epithelial germ cells, may develop toward hair structures.7
Desmoplastic Trichoepithelioma
Desmoplastic trichoepithelioma is a nonfamilial and usually solitary lesion.7 The
characteristic annularity and clinical hardness of this condition are not seen in any
other cutaneous tumour. It constant triad of microscopic findings – narrow strands of
basaloid tumour cells, keratinous cysts and desmoplastic stroma is unique in
dermatopathology.53
Pilomatricoma
Synonyms - Pilomatrixoma, calcifying epithelioma of Malherbe, benign calcifying
epithelioma3, Trichomatricoma47
Pilomatricoma was first described in 1880 by Malherbe as a calcifying
tumour believed to arise from the sebaceous gland.13,14 Turhan and Krainer were the
first to put forth the possibility of such a lesion arising from hair matrix cells.The term
pilomatricoma is relevant as it indicates the histogenesis of tumour.54
Pilomatricoma is a benign dermal or subcutaneous tumour, most
commonly affecting children and adolescents, more common in females, usually
35
occurs as a solitary firm lesion with predilection for head and neck and upper
extremities.49
Histopathology: The tumour is sharply demarcated and surrounded by a connective
tissue capsule.7 As a rule, two types of cells compose the islands of tumour-
basophilic cells and shadow cells.7Necrobiosis of matrix cells produces anucleate
shadow cells, while more complex necrosis will occasionally result in an area of
acellular debris.47In tumours of recent origin, numerous areas of basophilic cells are
present.7 Dystrophic calcification of epithelium occurs frequently and osseous
metaplasia of stroma is occasionally found with formation of both lamellar and woven
bone.47
Pilomatrix Carcinoma
It is a rare malignant counterpart of pilomatricoma. Pilomatrix carcinomas
are asymmetrical, cellular and infiltrative neoplasms .Features which are helpful in
making the diagnosis include asymmetry and poor circumscription, presence of
several markedly sized and variably shaped basaloid aggregations of tumor cells,
continuity of basaloid cells with the epidermis, extensive areas of necrosis ,
infiltrative growth pattern and presence of ulceration.7
Proliferating Trichilemmal Cyst
Synonyms - proliferating trichilemmal tumor 7, pilar tumor 55
Proliferating trichilemmal cyst is a benign adnexal tumour related to the isthmus of
hair follicle .55 About 90% of the cases occur on the scalp, with the residual 10%
occurring mainly on the back. More than 80% of the patients are women, most of
them elderly.7
36
Histopathology: The proliferating trichilemmal cyst is a well circumscribed tumour
composed of lobules of proliferating stratified squamous epithelium , surrounded by
thick hyalinised basement membrane ,with the centre of lobules showing trichilemmal
keratinisation and peripheral cell palisading .49 Squamous cells are bland or mildly
atypical with inconspicuous mitotic activity . Individual keratinisation and squamous
eddies are characteristic findings.Stromal reactive multinucleated giant cell reaction is
frequently present.49
Histogenesis – The tumour is analogous to that of outer root sheath as seen normally
at the follicular isthmus above the zone of sloughing of inner root sheath . 7
Malignant Proliferating Trichilemmal Tumor
Features of this malignant tumour include a combination of non scalp locations , size
> 5cm , recent rapid increase in size , infiltrative growth pattern , significant
cytonuclear atypia and brisk mitotic activity.49 In rare instances, malignant
transformation of proliferating trichilemmal cysts can take place.7
Trichilemmoma
Trichilemmomas are small solitary asymptomatic popular lesions found almost
exclusively on face. Although they appear to arise from follicular infundibulum they
differentiate towards the outer root sheath.5
Histopathology – Trichilemmomas are sharply lobulated epithelial neoplasm usually
in continuity with epidermis or follicular epithelium at several points. Tumour is
composed of squamoid cells showing glycogen vacuolation. Peripheral reserve cells
of the lobule tend to palisade resembling outer root sheath with a prominent basement
membrane remnisent of vitreous sheath of hair follicles.5,47 The overlying epidermis
37
shows hyperkeratosis with mild acanthosis uncommonly giving rise to cutaneous
horn.5 Multiple trichilemmomas occur in association with Cowden syndrome.5,7,49
Brownstein M.H et al in 1973 analysed 40 new cases of trichilemmomas and tried
to differentiate from other clear cell tumours of cutaneous origin which included clear
cell acanthoma, clear cell hidradenoma, tumours of sebaceous origin, metastasis from
renal cell carcinoma and BCC.56
Desmoplastic Trichilemmoma
Desmoplastic trichilemmoma is a histologic variant of trichilemmoma. Hunt S.J et al
in 1990 described 22 cases of trichilemmoma with desmoplasia which mimic invasive
carcinoma. 5,19
Trichilemmal Carcinoma
Trichilemmal carcinoma is a rare malignant counterpart of trichilemmoma defined by
Headington which has an indolent course.5,57
Tumors with Sebaceous Differentiation
Sebaceous tumours are relatively uncommon tumours of skin which include
benign and malignant forms.The characteristic histopathological feature that best
serves to identify a given lesion as sebaceous is the presence of sebaceous cells with
bubbly cytoplasm.58
Sebaceous Adenoma
Sebaceous adenoma is a benign tumour which usually presents as a slowing growing ,
pink or flesh coloured solitary nodule, predominantly on the head and neck of older
individuals.5
38
Histologically the tumour is composed of multiple sharply circumscribed sebaceous
lobules separated by septa.5The periphery of lobules may compress the surrounding
collagen ,producing an appearance resembling a capsule with pushing margins.55 The
lobules have a peripheral germinative layer of small cells, with mature sebaceous cells
centrally and transitional forms in between. This maturation is not as orderly or as
well developed as in normal sebaceous glands. The mature cells outnumber the darker
germinative cells.5
Sebaceoma
Synonyms – sebaceous epithelioma5,7
The term sebaceoma was coined by Ackerman. These tumours are usually solitary,
yellowish papulonodular on the face or scalp, but they are sometimes multiple
associated with Muir-Torre syndrome.5
Histologically there are random nests of basaloid cells with a random
admixture of sebaceous cells, either solitary or in clusters . The tumour is centered on
the upper and mid dermis. The small basaloid cells outnumber the mature sebaceous
component. Cysts and duct-like structures containing the debris of holocrine
degeneration may be present. The sebaceoma can exhibit an amazing diversity of
patterns.It is acknowledged that there is some overlap of this tumour with basal cell
carcinoma with sebaceous differentiation.5
Sebaceous carcinoma
Synonyms – Meibomian gland carcinoma15
Sebaceous carcinoma is a rare, aggressive, malignant tumour derived from
the epithelium of sebaceous glands
39
Sebaceous carcinomas are ocular or extra ocular. The Ocular sebaceous
carcinoma commonly arises from Mebomian glands of the upper eyelid. They are
more common and comprise 1% of all eye lid neoplasms. Extraocular lesions are rare,
common on head and neck region.They are seen in elderly females as rapidly growing
nodules, which may or may not be ulcerated. Rarely sebaceous carcinomas are
associated with Muir-Torre syndrome.5,7,15
Histologically, it is dermal tumour, with invasive asymmetrical growth
pattern.7 It is composed of lobules or sheets of cells showing variable sebaceous
differentiation usually at the centre of lobules. The nuclei are large, with large
nucleoli. There are scattered mitotic figures. Sometimes focal necrosis gives rise to
comedo-like pattern.5 Sebaceous carcinomas of the eye lids show a pagetoid spread
of malignant cells in the conjunctival epithelium or the epidermis of the skin of the lid
or both.7
Basically there are two broad classification schemes: 15
a. Classification based on growth patterns by
Rao et al. Ni et al.
1. Lobular 1. Squamoid
2. Comedo 2. Basaloid
3. Papillary 3. Adenoid
4. Mixed 4. Spindle cell
5. Differentiated
b. Classification based on degree of differentiation by Font15
1. Well differentiated tumor: contains many neoplastic cells with sebaceous
differentiation often towards centre of lobules.
40
2. Moderately differentiated tumor: only few areas of highly differentiated sebaceous
cells. Majority of tumor is composed of neoplastic cells with hyperchromatic nuclei
and prominent nucleoli and abundant basophilic cytoplasm.
3. Poorly differentiated tumor: majority of cells exhibit pleomorphic nuclei with
prominent nucleoli and scanty cytoplasm. Moderate increase in mitotic activity.
Sebaceous carcinomas of the eyelids quite frequently cause regional
metastases.7 Regardless of the location they are aggressive and have a tendency to
recur locally after surgical excision .15
Tumours with eccrine differentiation
Eccrine gland neoplasms are a complex group of neoplasms. They
demonstrate histologic similarity and a spectrum of eccrine acrosyringial, ductal and
secretory differentiation.17
Benign eccrine tumours
Eccrine Nevus/ Eccrine angiomatous nevus
Eccrine nevi are very rare. They may show a circumscribed area of
hyperhidrosis, a solitary sweat-discharging pore, or papular lesions in a linear
arrangement.7,17 Histologically, there may be hyperplasia of normal mature eccrine
secretory coils with single duct or an increase in both number and size of secretory
coils and multiple ducts.17
Eccrine angiomatous nevus is a rare form of benign organoid nevus
seen most commonly in palms and soles. The characteristic histological features
include an increased number of mature eccrine sweat glands and ducts as well as
interspersed vascular channels with occasional apocrine, pilar or adipose tissue
elements.7,59
41
Eccrine hidrocystoma17
Eccrine hidrocystoma was first described by Andrew Ross Robinson in 1893. This
lesion is usually solitary, small, semitranslucent, slightly blue intradermal nodule
occurring on the face. Histologically there is a single dilated cyst lined by two layers
of cuboidal cells. This lesion is due to the dilation of dermal straight duct (Between
the coiled duct and acrosyringium).
Syringoma
Syringoma was first described by Kaposi and Biesiadeki in 1872 as lympangioma
tuberosum multiplex.Darrier and Jacquet described the eruptive type of syringoma in
1887 as hydradenoma eruptives.17,60
Syringoma represents an adenoma of intraepidermal eccrine ducts. It
occurs predominantly in women at puberty or later in life.7 Syringomas may be
divided according to clinical presentation. Multiple syringomas of the lower eyelid are
the most common type. Localised syringomas are the second most common type.
They may occur on the cheeks, vulva, penis, dorsum of fingers or scalp where they
have been associated with alopecia. Milia-like, lichen planus-like and urticaria
pigmentosa-like lesions have been described.61
Histologically embedded in a fibrous stroma there are numerous small
ducts, the walls of which are lined usually by two rows of epithelial cells. In most
instances, these cells are flat. The lumina of the ducts contain amorphous debris.
Some of the ducts possess small, comma-like tails of epithelial cells, giving them the
appearance of tadpoles. In addition, there are solid strands of basophilic epithelial
42
cells independent of the ducts.7 Sometimes epithelial cells are keratinised and form
horn cysts.60
Histogenesis: Enzyme histochemical and electron microscopic studies have
established syringoma as a tumor with differentiation toward intraepidermal eccrine
sweat ducts.7,50,60
Eccrine poroma17
The eccrine poromas are a group of benign neoplasms originating from the uppermost
portion of intradermal eccrine sweat duct and the acrosyringium. They are classified
based on the histology and anatomic location as
A) Located entirely within the epidermis
Hidroacanthoma simplex
Poroid hidradenoma
Syringoacanthoma
B) Located within the epidermis and dermis
Eccrine poroma
C) Located entirely within dermis
Dermal duct tumour
Hidroacanthoma simplex17
Hidroacanthoma simplex is an intraepidermal eccrine poroma, first described in 1956
by Smith and Coburn. Histologically the lesion is composed of well defined
aggregates of small monomorphic cells with hyperchromatic nuclei and pale
eosinophilic cytoplasm located within the epidermis.
Eccrine poroma17
43
Eccrine poroma was first described by Hermann Pinkus et al in 1956. This solitary
lesion occurs most commonly on palms and soles.18 Clinically, it presents as firm,
raised or slightly pedunculated lesion.7
Histologically eccrine poroma arises within the lower portion of the
epidermis, from where it emanates downward into the dermis as tumor masses that
often consist of broad, anastomosing bands of epithelial cells. The tumor cells are
smaller than epidermal keratinocytes, have a uniform cuboidal appearance, a round,
deeply basophilic nucleus, and are connected by intercellular bridges. The tumour
shows ductal lumina. The border between tumour and richly vascularised stroma is
sharp.7
Dermal duct tumour17
Dermal duct tumour was first described by Winkelmann and McLeod. Histologically,
the tumour is located wholly within the dermis consisting of variously shaped tumour
islands containing ductal lumina.7,5,17
Eccrine spiradenoma: Eccrine spiradenoma is a well defined benign adnexal
neoplasm that was first described by Kersting and Helwig in 1956.62 Eccrine
spiradenoma usually occurs as a solitary intradermal nodule measuring 1 to 2 cm in
diameter.7
Histologically the tumour is composed of one or more, large sharply
delineated basophilic nodules in the dermis, unattached to epidermis.5 .On higher
magnification the cells are arranged in interwining cords. Two types of cells with
scant amount of cytoplasm are seen, dark cells at the periphery and pale cells at the
centre of aggregates which may be arranged partially around small lumina containing
PAS positive diastase resistant material.7
44
Histogenesis: Eccrine spiradenoma exhibits features of both the dermal duct and the
secretory segment of the eccrine sweat gland.7
Cylindroma
Cylindroma is a benign neoplasm occurs more often as a solitary dome shaped nodule
on head and neck. Multiple cylindromas are dominantly inherited and present as
multiple coalescing nodules on the scalp and forehead, referred to as turban
tumours.5,17
Histologically the tumor is composed of numerous islands of epithelial
cells of varied size and shapes, lying close together, separated by hyaline sheath
forming a jigsaw puzzle pattern. Two types of cells constitute the islands: cells with
small, dark-staining nuclei are present predominantly at the periphery of the islands,
often in a palisade arrangement, and cells with large, light-staining nuclei lie in the
center of the islands, showing luminal differentiation.7
Histogenesis: Cylindromas represent a tumor that show differentiation towards
secretory segment of apocrine origin and coiled duct region of eccrine origin. A more
recent study using monoclonal antibody is thought to be eccrine specific.5
Hidradenoma
Synonyms: Clear cell hidradenoma, clear cell myoepithelioma, eccrine sweat gland
adenoma of the clear cell type, solid cystic hidradenoma and eccrine acrospiroma.
Clear cell hidradenoma is a fairly common cutaneous neoplasm.
Clinically, this lesion is often a single dermal nodule measuring upto 2 cm in diameter
covered by intact skin.7,17 Histologically, the tumor is well circumscribed and may
appear encapsulated .7 The tumour is multilobated and composed of two types of
45
cells. One cell type is polygonal with small round to fusiform nucleus and basophilic
cytoplasm. The second cell type is round with small dark nucleus and abundant clear
to pale eosinophilic cytoplasm containing glycogen. Ductal lumina, squamous eddies,
keratinisation, occasional mitotic figures and apoptotic cells are often present.17
If the predominant cell type is clear or vacuolated, it is called clear cell
hidradenoma. If the neoplasm has both solid and cystic areas, it is called solid cystic
hidradenoma.17
Histogenesis: Nodular hidradenoma shows differentiation towards intraepidermal and
intradermal eccrine structures ranging from the poral epithelium to the secretory
segment.7
Chondroid Syringoma
Synonyms- Mixed tumour of skin
Nasse in 1892 described the first case of mixed cutaneous tumour.16 Later
in 1961, Hirsh and Helwig suggested the term “chondroid syringoma” for a group of
neoplasms that were previously called “mixed tumour of skin of salivary gland
type”.Clinically the lesion appears as a firm, dome shaped papule or nodule seen on
head and neck.17,63
Histologically, Chondroid syringomas are firm intradermal or
subcutaneous nodules.7 The tumour is a mixture of epithelial and mesenchymal tissue.
The tumour cells are of two different types: epithelial and myoepithelial cells. Two
types of chondroid syringomas can be recognized: one with tubular, cystic, partially
branching lumina, and the other with small, tubular lumina. The former type is much
more common than the latter.7,63
46
Chondroid syringoma with tubular, branching lumina shows marked
variation in the size and shape of the tubular lumina; it also shows cystic dilatation
and branching. Embedded in an abundant stroma, the tubular lumina are lined by two
layers of epithelial cells: a luminal layer of cuboidal cells and a peripheral layer of
flattened cells. Furthermore, there are aggregates of epithelial cells as well as single
epithelial cells widely scattered through the stroma. It appears that cells from the
peripheral cell layer of the tubular structures and from the solid aggregates proliferate
into the stroma..The abundant stroma in many areas has a mucoid, faintly basophilic
appearance. As a result of shrinkage of the mucoid substance, the fibroblasts and
epithelial cells that are scattered through it are surrounded by a halo, so that they
resemble the cells of cartilage.7
Histogenesis: They can be apocrine or eccrine. Electron microscopy demonstrates the
presence of both ductal and secretory lumina.7
Eccrine syringofibroadenoma7,17
Eccrine syringofibroadenoma is a rare benign lesion first described by Mascaro in
1963. Histologically the tumour consists of slender, anastomosing epithelial cords of
acrosyringeal cells, with or without formation of lumina, which are embedded in a
fibrovascular stroma.The tumour is contiguous but sharply demarcated from the
epidermis.
Histogenesis: Immunohistochemical studies and electron microscopy studies provide
evidence for acrosyringeal differentiation.
Tumours of apocrine differentiation
Benign tumours
47
Apocrine hydrocystoma5,7
Synonyms: Apocrine cystadenoma, cystic adenoma
Apocrine hydrocystoma occurs usually as a solitary, translucent, blue hued
nodule with a predilection for head and neck. Histologically the dermis contains a uni
or multi-loculated cyst lined by two layers of epithelial cells with occasional papillary
projections. The inner surface of the cyst is lined by a row of columnar secretory cells
showing decapitation secretion indicative of apocrine secretion and outer layer is
made up of flattened myoepithelial cells.
Hidradenoma papilliferum
Hidradenoma papilliferum usually presents as a solitary nodule and seen in
women and almost always found in the vulval and perineal regions.5
Histologically it is a well circumscribed tumour located in the dermis
surrounded by a fibrous capsule.Tumour has tubular and cystic structures with
papillary folds projecting into cystic structures. Usually, the lumina are surrounded by
a double layer of cells consisting of an inner layer of columnar secretory cells and of
an outer layer of small cuboidal cells with deeply basophilic nuclei, which are
myoepithelial cells.
Histogenesis: The apocrine nature of the secretion in hidradenoma papilliferum has
been established by histochemical, enzyme histochemical, and electron microscopic
examinations.7
Syringocystadenoma papilliferum
This tumour was first described by Werther in 1913.64 The largest series of cases have
been reported by Helwig and Hackney(100 cases).65 It is a rare benign tumour of
48
disputed origin.5,64,66The tumour has predilection for head and neck/W. Less common
sites of occurrence include chest, upper arms, back, trunk and thighs.5,64,65,66 It is
usually first noted at birth or in early childhood and presents as increases in size at
puberty, becoming papillomatous and often crusted.7
Histologically the epidermis shows varying degrees of papillomatosis.
One or several cystic invaginations extend downward from the epidermis. The upper
portion of the invaginations and, in some instances, the cystic invaginations are lined
by squamous, keratinizing cells similar to those of the surface epidermis.The lower
portion of the cystic invaginations contain numerous papillary projections lined by the
luminal row of high columnar cells occasionally showing active decapitation
secretion and outer row of cells consists of small cuboidal cells .5,7 The stroma that
surrounds the duct-like structures projects into papillations is usually rich in
inflammatory cells, most notably plasma cells.7,65
Histogenesis: In the view expressed by Pinkus most lesions of syringocystadenoma
papilliferum exhibit both apocrine and eccrine differentiation.7 Hence it is probable
that syringocystadenoma papilliferum arises from pleuripotential cells.7,65
Carcinomas of Apocrine and Eccrine Glands7
Carcinomas exhibiting apocrine and eccrine differentiation can be classified in several
different ways. One logical classification scheme distinguishes lesions based on
whether the carcinoma may frequently evolve from a benign lesion. In reality, this
group of tumors may derive either from a benign precursor through tumor progression
or de novo as a malignant lesion. In this group are malignant cylindroma, malignant
eccrine poroma, malignant eccrine spiradenoma, malignant nodular hidradenoma, and
malignant chondroid syringoma.
49
The second group comprises apocrine and eccrine carcinomas that appear
to have no benign precursor. In this group are carcinoma of apocrine glands, eccrine
adenocarcinoma, syringoid eccrine carcinoma, microcystic adnexal carcinoma,
mucinous (adenocystic) carcinoma, adenoid cystic carcinoma, and aggressive digital
papillary adenocarcinoma.
Malignant eccrine tumors
The classification of malignant eccrine tumours is one of the most confusing areas of
dermatopathology with identical tumours reported in the literature under three or
more designations.5
Eccrine Adeoncarcinoma ( classic type)17
Eccrine carcinoma or adenocarcinoma is a rare, highly malignant neoplasm with a
poor prognosis due to high incidence of metastatic disease. Although they may arise
on the palms or on the soles, they more commonly arise elsewhere, particularly in the
head and neck region. Histologically the architectural pattern varies from well-
differentiated ductal and papillary structures to solid anaplastic areas. Squamous
differentiation and spindle cells have been reported.
Eccrine porocarcinoma
Synonym: Malignant poroma
Eccrine porocarcinoma is a malignant neoplasm that may arise denovo or
in association with eccrine poroma.7,17Porocarcinoma was first described by Pinkus
and Mehregan as ‘epidermotropic eccrine carcinoma’.They present as verrucous
plaques or polypoidal growths which sometimes bleed with minor trauma.5
Mucinous carcinoma
50
It is rare eccrine carcinoma first described by Lennox et al and later
by Mendoza and Helwig. Histologically there are pools of mucin- containing solid
nests and cords of epithelial cells with focal ductal differentiation.17
Adenoid cystic carcinoma
It is one of the rarest type of eccrine carcinoma first described in 1975
by Boggio. Histologically, there is a cribriform, adenoid and focally cystic pattern in
association with solid epithelial islands. Mucinous degeneration of the stroma have
been reported. This indolent tumour also spreads into perineural spaces.7,17
Microcystic adnexal carcinoma
Synonyms: Sclerosing sweat duct carcinoma
It is a locally aggressive neoplasm most commonly found on the upper lip.17It is a
poorly circumscribed dermal tumor that may extend into the subcutis and skeletal
muscle.Two components within a desmoplastic stroma may be evident. In some areas,
basaloid keratinocytes are seen, some of which contain horn cysts and abortive hair
follicles; in other areas, ducts and gland-like structures lined by a two-cell layer
predominate.7
The presence of both pilar and eccrine structures allows
differentiation from desmoplastic trichoepithelioma and syringoma. Lack of
circumscription, deep dermal involvement and perineural involvement all aid in
diagnosis, since the cytology mimics benign adnexal neoplasms.7
Hidradenocarcinoma
51
Synonyms: Malignant acrospiroma3,5 malignant nodular hidraadenoma7, Clear cell
eccrine carcinoma5 , Clear-cell papillary carcinoma, clear-cell hidradenocarcinoma,
malignant clear-cell hidradenoma.3
This is a rare tumour with predilection for the face and extremities.5
Most cases of this carcinoma arise de novo, but some cases are associated with a
hidradenoma. Hidradenocarcinoma is composed of one or several tumour nodules,
which vary in size and shape. Focal tubular and ductal structures may be present.
Areas of necrosis en masse are common. Usually there is no connection between the
epidermis and the tumour. The same cell types as seen in hidradenoma are found in
hidradenocarcinoma.3 The term clear cell carcinoma is used in those with a prominent
clear cell change.5 Atypical cells with pleomorphic nuclei and mitotic figures may be
focally prominent.3
Histogenesis: Most neoplasms have apocrine differentiation, but some show eccrine
features.3
Carcinoma of apocrine glands
Synonyms: Apocrine adenocarcinoma, apocrine gland carcinoma3
Carcinoma of apocrine glands are rare tumors usually presents as single or
multinodular mass in the axilla or anogenital region .5 Apocrine carcinoma is thought
to arise from pre-existing apocrine (sweat) glands.3
The histologic picture is that of an adenocarcinoma that may be well,
moderately or poorly differentiated .7 Apocrine carcinoma is typically centered on the
deeper dermis and tends to spread into the subcutaneous fatty tissue .Extension into
the epidermis also occurs, occasionally in the form of extramammary Paget disease.3
52
In well-differentiated apocrine gland carcinomas, nuclear atypicality and
invasiveness are limited. Well-developed glandular lumina are present; these lumina
may be cystic and show branching. The cytoplasm of the tumor cells is strongly
eosinophilic.7 A key diagnostic criterion, decapitation secretion in the form of apical
snouts is usually recognizable but may be lacking in poorly differentiated tumours.3
There is variable mitotic activity./who In addition, the cytoplasm of the tumor cells
contain PAS-positive, diastase-resistant granules and often contains iron-positive
granules.5,7
In moderately or poorly differentiated apocrine gland carcinomas,
recognition of apocrine histopathologic features may be difficult to assess, although
even poorly differentiated tumors often demonstrate regions with prominent apocrine
differentiation.7
Benign Pigmented Lesions and Malignant Melanoma
Melanocytic proliferations are composed of one or more of three related types of
cells: melanocytes, nevus cells or melanoma cells, each of which may be located in
the epidermis or in the dermis.
Melanocytes are solitary, dendritic cells with small regular nucleus. Nevus
cells are rounded or spindle shaped cells arranged in clusters with small regular
nucleus. Melanoma cells are rounded or spindle shaped arranged in clusters and
sheets with large irregular hyperchromatic nucleus.4
Benign tumors of nevus cells are called melanocytic nevi, while
malignant tumors are called malignant melanomas and the cells of these lesions are
called as melanoma cells. Melanocytic lesions are of importance primarily because of
53
malignant melanoma, which is single most common potentially lethal neoplasm of
skin.4
Melanocytic nevus
Melanocytic nevus is generally considered to be a benign neoplastic proliferation of
melanocytes. Melanocytic nevi are only rarely present at birth. Most nevi appear in
adolescence and early adulthood. Melanocytic nevi are defined by the presence of
nevus cells, which, even though they are melanocytes, differ from ordinary
melanocytes by being arranged at least partially in clusters or nests, by the tendency
to round rather than dendritic cell shape and a propensity to retain pigment in their
cytoplasm.4 Many nevi appear to be clonal.12
There are transitional stages in the life cycle of nevi, which are believed to
start out as junctional nevi, then compound nevi and after having become intradermal
nevi, undergo involution.4
Junctional nevi
It presents as a well circumscribed brown to black macule which can appear
any where on the body surface and appears during childhood or early adolescence.12
Histopathologically it is composed of nevus cells that lie in well-
circumscribed nests either entirely within the lower epidermis or bulging downward
into the dermis but still in contact with the epidermis. The nevus cells in these nests
generally have a regular, cuboidal appearance, although they are occasionally spindle-
shaped. Varying amounts of melanin granules are seen in the nevus cells.4
Compound nevi
They occur more commonly in children and adolescents.12Clinically, a
compound nevus is a pigmented papule or a plaque.4
54
Histologically, a compound nevus possesses features of both a
junctional and an intradermal nevus. Nevus cells in the upper, middle, and lower
dermis may present characteristic morphologic variations called types A, B, and C,
respectively. Usually, the type A nevus cells in the upper dermis are round to cuboidal
and show abundant cytoplasm containing varying amounts of melanin granules.
Melanophages are occasionally seen in the surrounding stroma. The cells in the mid-
dermis usually are type B cells. They are smaller than the type A cells, display less
cytoplasm and less melanin, and generally lie in well-defined aggregates or cords.
Type C nevus cells in the lower dermis tend to resemble fibroblasts or Schwann cells,
because they are usually elongated and possess a spindle-shaped nucleus. They often
lie in strands and only rarely contain melanin.4
Intradermal nevus
It is the most common type of melanocytic nevi and vast majority are found
in adults.12Intradermal nevi show essentially no junctional activity.4 Nevus cells are
confined to the dermis where they are arranged in nests and cords. Multinucleate cells
may be seen. In the deeper parts of the lesion nevus cells may assume a neuroid
appearance.4
Baloon cell nevus
This is a rare lesion clinically indistinguishable from ordinary nevus. 12 The
ballooning is believed to develop from melanosome degeneration.28
Histologically, nevus may be compound or dermal and the swollen nevus
cells have clear cytoplasm and a central hyperchromatic nucleus. The diagnosis is
restricted to lesions containing over 50% of balloon cells and not nevi showing focal
balloon cell changes.12,28
55
Halo nevus
It is characterised by presence of depigmented halo several cms in width,
around a melanocytic nevus.12 Most persons with are children or young adults, and
the back is the most common site.4
Histologically, there is dense lymphocytic infiltrate within the dermis and
nevus cells are seen surviving in nests or singly among lymphocytes. Macrophages
are also present in the infiltrate. The depigmented halo shows an absence of melanin
pigment and melanocytes in the basal layer. Rarely a halo nevus is devoid of
inflammatory cells. 12 At a later stage, only a few, and finally no distinct nevus cells
can be identified. 4
Spitz nevus
Synonym: Spindle cell nevus, epithelioid cell nevus, benign juvenile melanoma 12
The Spitz nevus, named after Sophie Spitz, who first described it in 19484,12.
The lesion usually is solitary and is encountered most commonly on the lower
extremities and face. In most instances, it consists of a dome-shaped, hairless, small
pink nodule. In 95% of the patients, the size of the tumor is <1 cm. Its differentiation
from a melanoma can often be very difficult and occasionally even impossible.4
Histologically, most Spitz nevi are compound, 5-10% are junctional and
20% are intradermal lesions.
The major diagnostic criteria include:12
1. Symmetrical appearance of lesion
2. Cell type- epitheloid and/or spindle cells
3. Maturation of nevus cells
4. Lack of pagetoid spread of single melanocytes
56
5. Coalescent, pale pink Kamino bodies.
Minor criteria
1. Junctional cleavage
2. Pseudoepitheliomatous hyperplasia
3. Superficial dermal edema and telangiectasia
4. Giant nevus cells (multinucleate and uninucleate)
5. Absence of pleomorphism
Congenital melanocytic nevus
A congenital melanocytic nevus may be defined as a lesion present at birth
and containing nevus cells. Congenital nevi are found in about 1% to 2% of newborn
infants.4 Majority are less than 10mm in diameter.12 Giant congenital nevi have the
distribution of a garment( garment nevi).4
Large congenital melanocytic nevus, defined as those that are at least
20cm in largest diameter, have been reported to increase the risk for the development
of malignant melanoma.67 These melanomas are non-epidermal in origin.12
In the study done by Illig L et al, the author has set the limit for small
congenital melanocytic nevus arbitrarily at 10cm and concluded that they are potential
precursors of melanoma which are preferentially epidermal in origin.68
Histopathology: Congenital nevi may be junctional, compound or intradermal in type,
depending on the age at which they are removed. Nevi removed after neonatal period
show the presence of nevus cells between collagen bundles singly or in Indian file or
extension of nevus cells around nerves, vessels and adnexae.12
Blue nevus12
It is a small slate blue to blue black macule or papule found in extremities,
57
acquired after infancy.
Histologically, the common blue nevus is composed of elongated,
sometimes finely branching melanocytes in the interstices of dermal collagen in upper
and middermis. Laterally the lesion merges with the dermis without a clear margin
and macrophages containing melanin are often found.
The cellular blue nevus is composed of dendritic melanocytes with islands of
epitheloid and plump spindle cells with abundant pale cytoplasm and usually little
pigment. Heavily pigmented varients do occur.
Dysplastic nevus
Dysplastic nevi are clinically distinctive, histologically characteristic and biologically
relevant.69The melanoma susceptible family members are prone for dysplastic
melanoma syndrome.70
Histologically they show three characteristic features: lentiginous
hyperplasia, random cytologic atypia and a stromal response. A fourth feature,
architectural atypia, is generally regarded as a diagnostic requirement.12
Lentiginous hyperplasia: The proliferation of melanocytes occurs singly and also in
nests along the basal layer. Uneven distribution pattern of junctional component is
called “junctional nest disarray”. The individual cells are spindle shaped with scanty
cytoplasm with shrinkage artifact.
Random cytological atypia: Presence of occasional cells with enlarged
hyperchromatic nuclei with prominent nucleoli, which progresses with increase in age
of patients.
Stromal response: Lamellar and concentric fibroplasia of papillary dermis with
proliferation of dermal dendrocytes.
58
Architectural atypia: There is ‘shoulder phenomenon’, that is peripheral extension of
junctional component beyond dermal component.12
Malignant melanoma
Melanomas arise from epidermis and these may be in situ or may be invasive.
Invasive melanoma may be tumorigenic or non-tumorigenic.
All major types of melanoma originate almost invariably from
melanocytes at the epidermal-dermal junction, also can occur in pre-existing
melanocytic nevi.4 Clark and colleages introduced the concept of radial and vertical
growth phase in the evolution of malignant melanoma.12Malignant melanoma of skin
is rare and has lower incidence among Indians.71 Melanomas may mimic carcinomas,
sarcomas, stromal tumours, lymphomas, plasmacytomas and germ cell tumours.72
Classification of malignant melanoma4
Radial Growth Phase (RGP)
Non-tumorigenic melanoma
In situ or microinvasive
Superficial spreading melanoma (SMM)
Lentigo maligna melanoma (LMM)
Acral lentiginous melanoma (ALM)
Unclassified radial growth phase (URGP)
Vertical Growth Phase (VGP)
Tumorigenic melanoma
No RGP compartment
Nodular melanoma
RGP compartment present (may be SSM, LMM, ALM, URGP)
Usual vertical growth phase
Desmoplastic
Neurotropic
59
Other variants (e.g. nevoid/minimal deviation melanoma, ‘balloon cell’,
‘amelanotic’, ‘spindle cell’, malignant blue nevus etc)
Superficial spreading melanoma (SMM)4
Superficial spreading melanoma (SSM), also referred to as pagetoid melanoma
is the most frequent form of melanoma (about 70% of all cases), and may therefore be
regarded as the common or prototypic form of melanoma. The most frequently
involved sites are the upper back, especially in men, and the lower legs, especially in
women. Histologically, uniformly rounded, large melanocytes are scattered in
pagetoid pattern throughout the epidermis and lie in nests in lower epidermis and
singly in upper epidermis. The individual cells have large hyperchromatic nuclei and
abundant cytoplasm, containing varying amount of melanin. The epidermis is is
irregularly thickened and thinned and dermis shows melanophages and inflammatory
infiltrate.
Lentigo maligna melanoma
Previously referred to as melanosis circumscripta preblastomatora of
Dubrevilh and also as melanotic freckle of Hutchinson. Lentigo maligna occurs on
sun exposed cutaneous surfaces of elderly, commonly over face and rarely over
forearms and lower legs accounts for 10% of melanomas.
Lentigo maligna melanoma develops from lentigo-maligna. The lesion starts
as pigmented macule that gradually extends peripherally and may attain several
diameter with no induration. Invasive malignancy (VGP) is characterised by
thickening of lesion with development of elevated plaques or discrete nodules.
Histologically, in early stage, hyperpigmentation of basal layer, with some
60
areas showing extension to higher areas of epidermis is seen. In advanced lesions
basal melanocytes are markedly increased and may exceed the basal keratinocytes.
The melanocytes are haphazardly arranged along dermo epidermal junction and are
spindle shaped with atypical enlarged hyperchromatic nuclei. These atypical
melanocytes frequently extend along the basal layer of hair follicles and some nesting
of melanocytes in the basal layer may be seen. The epidermis is frequently flattened.
The upper dermis, in addition to showing solar degeneration, contains melanophages
and a band like infiltrate which extends beyond the altered epidermis.4
Acral lentiginous melanoma (ALM)
Acral melanoma occurs on the hairless skin of the palms and soles and in the ungual
and periungual regions, the soles being the most common site. It shows irregular,
uneven pigmentation with definite borders.
Histologically, there is a radial growth phase which is characterised by a
lentigenous pattern of atypical melanocytes, with some nesting.12The histologic
picture in advanced cases is similar to that of lentigo maligna except for irregular
acanthosis.4
Nodular melanoma4
Nodular melanoma by definition contains only tumorigenic vertical growth
and, because of this, has a poorer prognosis. A nodular melanoma starts as an
elevated, variably pigmented papule that increases in size quite rapidly to become a
nodule, and often undergoes ulceration.
Hispopathology of nodular melanoma and common vertical growth phase melanoma:
In a typical tumorigenic melanoma, there is contiguous proliferation of neoplastic
61
melanocytes in the dermis forming a tumor mass that is larger than the largest nest in
the overlying epidermis.
The tumor mass is comprised of uniformly atypical cytologically fully
malignant and mitotically active cells usually growing in confluent nests or in sheets.
Two major types of cells are recognized, an epithelioid and a spindle-shaped cell type.
Many tumors show both types of cells, but usually one type predominates.
Desmoplastic melanoma
Desmoplastic melanomas are often non -pigmented and stubbornly recurrent usually
seen in the head and neck region.12The melanoma cells are elongated, amelanotic and
are embedded in a markedly fibrotic stroma.
Neurotropic melanoma is often a variant of desmoplastic melanoma . There
are fascicles of desmoplastic melanoma that have invaded cutaneous nerves, usually
in a spindle-cell vertical component with fibrosis.4
Breslow thickness of tumour: It is the single most important factor in predicting
survival of patients. The thickness of tumour is measured from granular layer to the
deepest tumour cell. Melonomas <0.76mm are thin melanomas and generally have
excellent prognosis.12
Clark’s level of invasion:4,12 Has a prognostic and descriptive value.
Level 1- confined to epidermis
Level 2 –Invasion into papillary dermis
Level 3 –Invasion into papillary and reticular dermal interphase
Level 4 – Invasion into reticular dermis
Level 5 – Invasion into subcutaneous fat.
62
MATERIALS AND METHODS
SOURCE OF DATA: All the biopsies, specimens and reference materials submitted
to the department of Pathology, KIMS, Hubli for histopathological study during the
period from July 2005 to June 2010 (Three and half year retrospective and one and
half year prospective study).
Data for retrospective study is obtained from departmental records, tissue
blocks and slides.
Data for prospective study is obtained from clinical records and tissue
specimens.
METHODS OF COLLECTION OF DATA: Clinical data is obtained from hospital
records and tissue specimens received in the department. Nature of specimen was
noted. Specimens were fixed in 10% formalin for 12-36 hours and the gross features
were examined. Extent of sampling depended on the size of tumor as follows.
1. Specimens measuring 3 mm or less were submitted in toto.
2. Specimens measuring 4-6 mm were cut through the centre and both halves
submitted for processing.
3. Specimens measuring 7 mm or more, a 2-3 mm slice from centre was cut and
submitted for processing.
4. For larger malignant lesions, 2-4 sections from tumor and 4 or more sections from
surgical margins were taken.
Further, tissue was processed and embedded in paraffin blocks. Sections of
3 to 5micron thickness were taken and stained with hematoxylin and eosin and
studied.
63
INCLUSION CRITERIA:
Tumours of epidermis along with melanocytic tumours and tumours of skin
appendages without restricting the study to a particular age limit.
EXCLUSION CRITERIA:
i. Mesenchymal tumours
ii. Hematological tumours
iii. Skin secondaries
iv. Non neoplastic lesions
ETHICAL CLEARANCE: Ethical clearance has been obtained from Ethical
Committe of KIMS, Hubli.
STATISTICAL METHODS APPLIED:
Following statistical methods were applied in the present study.
1. Number and percentage
2. Chi-square test
3. Descriptive statistics.
64
RESULTS AND OBSERVATIONS
During the period of 5 years from July 2005 to June 2010, there were 218
cases which presented as skin tumours and out of these, 82 happened to be cysts and 1
pseudoepitheliomatous hyperplasia which were excluded from the study and the
remaining 135 were tumours of skin.
Figure 6: Incidence of benign and malignant tumours of skin.
Benign
Malignant
34%
66%
Out of the 135 cases, 46 were diagnosed as benign and 89 as malignant
tumours of skin constituting 34% and 66% respectively. The ratio of malignant to
benign tumours was 1.93:1
Table 1: Incidence of skin cancer
Total number of cancers
Number of skin cancers
Percentage
6,803
89
1.3
65
Department of Pathology, KIMS caters to a large area in and around Hubli.
The department has received a total of 25,658 specimens for HPR during the study
period .Out of these 6,803 were diagnosed as cancers of various sites in the body and
cancers of skin accounted for 89 cases (1.3%) of this.
Table 2: Distribution and incidence of benign and malignant tumours of skin
No of epidermal
tumours
No of adnexal
tumours
No of melanocytic
tumours
Benign 11 (8%) 25 (19%) 10 (7%)
Malignant 77 (57%) 6 (4.5%) 6 (4.5%)
Total No of cases 88 31 16
χ2 =53.9 p <0.001 (Highly significant)
Out of 135 skin tumours, malignant epidermal tumours were most common
(57%) , followed by benign tumours of epidermal appendages (19%), benign tumours
of epidermis (8%), benign melanocytic tumours (7%) and malignant melanoma and
malignant adnexal tumours (4.5% each)
Table 3: Age incidence of benign tumours of skin.
10-19 20-29 30-39 40-49 50-59 60-69 70-79 80-89 Total
Epidermal
Verruca vulgaris 2 - 1 1 - 2 - - 6
Seborrheic keratosis - - 1 1 - 2 1 - 5
Adnexal- Hair
follicle
Proliferating
trichilemmal tumour
1 1 1 2 - 2 - - 7
Pilomatricoma 1 1 2 - - - - - 4
Trichoepithelioma - - - - 1 - - 1 2
Sweat gland
Hidradenoma 1 - - 1 2 1 1 - 6
66
Syringoma - 1 - - - - - - 1
Cylindroma - - 1 - - - - - 1
Chondroid
syringoma
- - - 1 - - - - 1
Syringocystadenoma
papilliferum
- - 1 - - - - 1
Apocrine
hidrocystoma
- - - - - 1 - - 1
Sebaceous gland
Sebaceoma - - - - 1 - - - 1
Melanocytic
Nevocellular nevus 1 3 3 2 1 - - - 10
Total 6 6 10 8 5 8 2 1 46
In the present study the peak incidence was between 3rd and 5th decade (52%).
Table 4: Age incidence of malignant tumours of skin
10-19
20-29
30-
39
40-
49
50-59
60-
69
70-
79
80-
89
Total
SCC - 2 7 8 13 16 3 - 49
Verrucous
Carcinoma
- 2 - 2 2 1 1 - 8
BCC - - 1 3 5 4 6 1 20
Malignant
melanoma
- 1 - - 1 3 1 - 6
Adnexal
carcinoma
1 1 - 1 - 2 1 - 6
Total 1 6 8 14 21 26 12 1 89
In the present study the peak incidence was between 5th and 7th decade (68.5%).
67
Table 5: Sex incidence of benign and malignant tumours of skin
Sex Number of cases Percentage
Male 83 61.5
Female 52 38.5
Total 135 100
The study showed there was male predominance with the male to female ratio
of 1.57: 1.
Figure 7: Sex incidence of benign and malignant tumours of skin
Benign tumours of skin and adnexae
In the present study, benign tumours accounted for 46 (34%) out of 135 skin
tumours.
61%
39%
Male
Female
68
Table 6: Incidence of different benign tumours of skin.
Tumours
Number of cases Percentage
Epidermal
11
24
Verruca Vulgaris 6 13
Seborrheic keratosis 5 11
Adnexal
25
54
Hair follicle
differentiation
13 29
Sweat gland
differentiation
11 23
Sebaceous
differentiation
1 2
Melanocytic
10
22
Intradermal nevus 9 20
Compound nevus 1 2
Total No of cases
46 100
In the present study benign adnexal tumours formed the majority (54%)
followed by epidermal tumours (24%) and melanocytic nevus(22%)
Benign tumours of epidermis
1 . Verruca Vulgaris: In the present study 6 cases (13%) of verruca vulgaris were
encountered. Three cases were located on the sole of foot, 1 on leg, 1 on thigh and 1
on the vulva. The study showed male predominance with male to female ratio of 2:1.
Ages ranged from 10-65years. All the 6 cases showed acanthosis, hyperkeratosis,
69
parakeratosis and varied degree of papillomatosis. Koilocytic change was seen in 3
cases.
2 . Seborrheic keratosis: In the present study 5 cases (11%) of Seborrheic keratosis
were encountered. There were 3 men and 2 women, with male to female ratio of
1.5:1. Ages ranged from 38-72 years. 4 cases were located on the trunk and one on
the ear. All the 5 cases showed acanthotic type of seborrheic keratosis . Acacthosis
was seen in all 5 cases where as hyperkeratosis, papillomatosis and horn cysts were
seen in variable degree. In all cases basaloid cells showed melanin pigment within the
cytoplasm.
Benign melanocytic tumours:
1 . Intradermal nevus: In this study 9 cases of intradermal nevus were seen. All 9
cases were seen in head and neck region. Peak incidence was seen between 20-40
years (60%) .Histologically the dermis showed nests, cords and sheets of nevus cells
showing maturation. The cells showed varied amount of intracytoplasmic melanin
pigment. Also seen were few melanophages in the dermis.
2 . Compound nevus: One case was encountered in the study. The patient was a 12
year old female having a nodule over ear. Histologically epidermis was thinned out
and showed junctional activity with dermal component of nevus cells showing
maturation.
Malignant tumours of skin.
In the present study, malignant tumours accounted for 89 (66%) out of 135
skin tumours
70
Table 7: Incidence of different malignant tumours of skin.
Tumour Number of cases Percentage
Epidermal Squamous cell carcinoma
Verrucous Carcinoma
Basal cell Carcinoma
49
8
20
55
9
22.5
Adnexal Hidradenocarcinoma
Sebaceous Carcinoma
Apocrine Carcinoma
Malignant proliferating
trichilemmal tumour
2
2
1
1
2.3
2.3
1.1
1.1
Melanocytic Malignant melanoma
6
6.7
Total No of cases
89
100
In the present study squamous cell carcinoma was commonest (55%) ,
followed by basal cell carcinoma (22.5%), verrucous carcinoma(9%) and malignant
melanoma and malignant adnexal tumours(6.8%).
71
Figure 8: Site distribution of malignant tumors of skin
Diagnosis(abbreviation) Symbol Total
cases(percentage)
Squamous cell carcinoma(SCC) 49(55%)
Verrucous carcinoma (VC) 8(9%)
Basal cell carcinoma (BCC) 20(22.5%)
Malignant Melanoma (MM) 6(6.7%)
SCC(12) MM(5)
BCC(1)
SCC(2)
VC(4)
VC(1)
BCC(17)
BCC(2)
SCC(12)
SCC(1)
SCC(19) SCC(2)
SCC(1)
VC(3) MM(1)
72
Malignant tumours of epidermis
Squamous cell carcinoma
In the present study 49 cases of SCC were encountered accounting for 55% of
skin cancer.
Table 8: Location of SCC in comparison with males and females
Site
Males
Females
Total
No
%
No
%
No
%
Head and
neck
8
21
4
40
12
24
Extremities
11
28
4
40
15
31
External genetalia
18
46
1
10
19
39
Trunk
2
5
1
10
3
6
Total
39
80
10
20
49
100
x2 =4.59 p=0.20
In the present study maximum number of cases occurred over external
genetalia (penis) in males and head and neck and extremities in females.
73
Figure 9: Location of Squamous cell carcinoma in males and females
Table 9: Age and sex incidence of squamous cell carcinoma.
Age in years
Males Females Total
No
%
No
%
No
%
20-29
1 2.5 1 10 2 4
30-39
5 13 2 20 7 14
40-49
7 18 1 10 8 16
50-59
10 25.5 3 30 13 27
60-69
14 36 2 20 16 33
70-79
2 5 1 10 3 6
Total
39 80 10 20 49 100
The peak incidence was in 7th decade in males and 6th decade in females
74
Figure 10: Age incidence of SCC in males and females
Figure 11: Sex incidence of squamous cell carcinoma
80%
20%
Males
Females
In the present study there was male preponderance (80%) with male to female
ratio of 4:1.
75
Table 10: Conventional grading of squamous cell carcinoma
Grade Number of cases Percentage
Well 35 71
Moderate 13 27
Poor 1 2
Table 11: Broder’s grading of squamous cell carcinoma
Grade Number of cases Percentage
1 32 65.3
2 9 18.4
3 7 14.3
4 1 2
All squamous cell carcinomas were graded conventionally as well, moderate
and poorly differentiated and this was compared with Broder’s grading. Majority of
the squamous cell carcinomas were well differentiated (71%). All the 32 cases of
Broder’s grade 1, 7 cases of grade 3 and 1 case of grade 4 belonged to well, moderate
and poorly differentiated variety of the conventional grading system respectively. Out
of 9 cases of Broder’s grade 2, 3 were well differentiated and 6 were moderately
differentiated according to the conventional grading system.
Verrucous carcinoma: In the present study 8 cases were encountered. Patients’ age
ranged from 25 to 75 years.
Microscopically these tumours showed a classical exo and endophytic growth.
The downgrowths of the tumours were bulbous with varying depths with an intact
76
basement membrane. The squamous cells stained lightly with eosin and nucleus was
small. Cellular atypia, mitotic activity and other characteristics of malignancy were
absent (Fig.No.24).
Table 12: Sex incidence of verrucous carcinoma
Sex Number of cases Percentage
Males 6 75
Females 2 25
In this study majority of cases occurred in males (75%) with male to female
ratio of 3:1.
Table 13: Location of verrucous carcinoma
Site Number of cases Percentage
Foot 4 50
Lip 3 38
External genitalia 1 12
The sites of occurrence of these tumours according to decreasing order of
frequency were foot (50%), lip (38%) and external genitalia (12%).
77
Basal cell carcinoma:
In the present study 20 cases of basal cell carcinoma were encountered and
accounted for 22.5% of all the malignant tumours of skin. Peak incidence was in 8th
decade. Mean age of patients was 60.6 years .
Table 14: Sex incidence of basal cell carcinoma
Sex Number of cases Percentage
Males 11 55
Females 9 45
In this study a male preponderance was noted with male to female ratio of 1.2: 1.
Table 15: Location of basal cell carcinoma
Site Number of cases Percentage
Head and neck Eye lid Nose
Forehead Cheek
Ear front Scalp
Post auricular
17 7 1 3 3 1 1 1
85 41 5.9
17.6 17.6 5.9 5.9 5.9
Trunk 2 10
Limb 1 5
85% of cases of basal cell carcinoma were located on head and neck region
and majority of these (41%) were seen in the eye lids.
78
Figure 12: Location & number of cases of basal cell carcinoma in head and neck.
Table 16: Histological types of basal cell carcinoma
Type Number of cases Percentage
Pigmented BCC 8 40
Solid BCC 4 20
Adenoid BCC 4 20
Keratotic BCC 2 10
Infiltrating BCC 1 5
Basosquamous carcinoma 1 5
In the present study marked melanosis was seen in the tumour tissue in 8 cases
and these were designated as pigmented basal cell carcinoma. Basal cell carcinomas
showing no differentiation were categorized as solid BCC. Adenoid BCC showed
cellular arrangement suggesting tubular structures. The cells were arranged in
1
3
7
1
3
1
1
79
intertwining strands resulting in a lacelike pattern. Keratotic BCC showed
keratinisation in the form of horn cysts. In the infiltrating variant of BCC the basaloid
cells were arranged in cords and showed deep infiltration in the dermis. One case of
basosquamous carcinoma was found in which the basal cell carcinoma existed with
squamous cell carcinoma and it was seen as an ulcer over the scalp in a 45 year old
male.
Figure 13: Histological types of basal cell carcinoma
0
1
2
3
4
5
6
7
88
4 4
2
1 1
Num
ber o
f cases
Histological types of basal cell carcinoma
Malignant melanoma:
In this study 6 cases of malignant melanoma were encountered and it
accounted for 6.7% of all malignant skin tumours. The youngest was 28 years and
oldest, 70 years. Majority of cases were between 60-79 years (66.66%).
80
Table 17: Sex incidence of malignant melanoma.
Sex Number of cases Percentage
Male 5 83
Female 1 17
Sex distribution showed a significant difference with 83% males and 17%
females showing male predominance.
Table 18: Location of malignant melanoma
Site Number of cases Percentage
Sole 5 83
Ear 1 17
The most common site was sole (5 cases – 83%) and one case (17%) occurred
in the ear lobe.
Table 19: Clark’s grading of malignant melanoma
Grade Number of cases Percentage
Grade 1 0 -
Grade 2 0 -
Grade 3 1 17
Grade 4 5 83
Grade 5 0 -
81
83% of cases showed infiltration upto reticular dermis (Clark’s grade 4) and
17% of cases showed infiltration upto papillary and reticular dermal interphase
(Clark,s grade 3).
Histologically all cases showed junctional activity at the dermoepidermal
junction. Both epithelioid and spindle shaped cells were seen. 2 cases were of
epitheloid cell type and 4 cases were of mixed pattern having both epithelioid and
spindle cells. The cells were arranged in nests and sheets with pleomorphic nuclei and
prominent eosinophilic nucleoli. Varying amount of intracytoplasmic pigment was
seen in the tumour cells and macrophages. Pagetoid spread to epidermis was seen in 2
cases and necrosis was seen in 1 case. . Metastatic spread to lymph nodes was seen in
2 cases (Fig.No.17).
Adnexal tumours of skin.
In the present study 31 cases of skin adnexal tumours were encountered, out of
which 25 were benign and 6 were malignant.
82
Table 20: Incidence of skin appendageal tumours
Number of benign tumours
Number of malignant tumours
Total number
of tumours
Hair follicle differentiation 13(52%) 1(16.7%) 14(45%)
Sweat gland Differentiation 11(44%) 3(50%) 14(45%)
Sebaceous differentiation 1(4%) 2(33.3%) 3(10%)
Total No of cases 25(80.6%) 6(19.4%) 31
χ2=5.68, p= 0.05 (significant)
In the present study benign tumours formed the majority (80.6%).
Among the benign tumours the occurrence of hair follicle tumours (52%) was
highest followed by sweat gland tumours (44%) and sebaceous tumours (4%).
Among the malignant tumours sweat gland carcinoma was the most common
type (50%) followed by sebaceous carcinoma (33.3%) and hair follicle carcinoma
(16.7%).
Malignant tumours were more than benign in sebaceous group of tumours,
where as benign were more than malignant in hair follicle and sweat gland tumours.
83
Figure 14: Incidence of benign and malignant skin adnexal tumours.
0
2
4
6
8
10
12
14
Hair follicle tumours
Sweat gland tumours
Sebaceous gland tumours
13
11
11
32
Num
ber o
f cases
Types of adnexal tumours
Benign
Maliganant
Benign adnexal tumours
Hair follicle tumours:
Table 21: Incidence of benign hair follicle tumours
Tumours No.of cases
in males No.of cases in
females Total No. of
cases Percentage
Proliferating
trichilemmal tumour
Pilomatricoma
Trichoepithelioma
2
1
-
5
3
2
7
4
2
54
31
15
Total 3 10 13 100
84
Hair follicle tumours constituted 52% of the benign adnexal tumours out of
which majority (54%) of cases were proliferating trichilemmal tumour followed by
pilomatricoma (31%), trichoepithelioma (15%) .Majority of cases were seen in
females with male to female ratio of 1:3.33.
Proliferating trichilemmal tumour: There were 7 cases in the study accounting for
54% of tumours, out of which 5 were females and 2 males, with male to female ratio
of 1:2.5. Age range was 14-60 years. Most common site was scalp (5 out of 7 cases).
Other 2 occurred in leg and axilla.
Histologically, all cases showed a well defined tumour composed of squamous
cells showing abrupt keratinisation and peripheral palisading. The tumour cells
showed mild pleomorphism as well as dyskeratosis (Fig No.32). Calcification was
seen in 4 cases. One case showed the presence of squamous eddies. There was one
case of pilar cyst with proliferating trichilemmal tumour in a 60 year old male who
presented with scalp swelling which histologically showed the presence of
calcification and cholesterol clefts along with squamous islands.
Pilomatricoma: In the present study 4 cases were encountered accounting for 31% of
cases, out of which 3 were females and 1 male with male to female ratio being 1:3.
These occurred at the age of 14, 26, 30 and 38 years. 2 cases occurred on face, one in
axilla and one over leg . In one case, a 30year old female presented with a recurrence
of pilomatricoma in the axilla after 2 years of excision which was grossly a 7cm
diameter calcified mass (Fig. No. 19)
85
Histologically the tumours were well circumscribed, composed of islands of
basophilic cells and shadow cells (Fig. No.31). Calcification was seen in 2 cases and
one case showed giant cell reaction to keratin.
Trichoepithelioma: Two cases were encountered in the study. Both were females
aged 50 and 80 years, presented with nodule over face.
Histologically, showed islands of basaloid cells in the dermis with peripheral
palisading of cells. There was no connection of these islands with the epidermis. Horn
cysts and presence of fibrous stroma was noted (Fig. No 30).
Sweat gland tumours:
Table 22: Incidence of benign sweat gland tumours
Tumours No. of cases
in males No. of cases
in females Total No. of
cases Percentage
Hidradenoma Syringoma Chondroid syringoma Apocrine hidrocystoma Cylindroma Syringocystadenoma
papilliferum
2 - 1 1 - 1
4 1 - - 1 -
6 1 1 1 1 1
55 9 9 9 9 9
Total 5 6 11 100
Sweat gland tumours constituted 44% of benign adnexal tumours out of which
55% of cases were of hidradenoma followed by 9% each of syringoma, chondroid
syringoma, cylindroma, apocrine hidrocystoma, syringocystadenoma papilliferum and
apocrine carcinoma. The male to female ratio was 1:1.2 with reference to table 22.
These tumours may show eccrine or apocrine differentiation.
86
Hidradenoma: 6 cases were encountered in the study, out of which 4 were females
and 2 males with male to female ratio of 1:2. Age range was 18-75 years. Four cases
were seen on the trunk and 2 on the face. Histologically the tumour showed well
circumscribed lobular mass with cystic change composed of clear cells and
eosinophilic cells and the cytoplasm clear cells showed PAS positivity (Fig.No27)
.One of the case showed extensive squamous differentiation.
Syringoma: One case was noted in 27 year old female with a nodule over eye lid.
Histologically the epithelial cells were arranged in nests and tubules showing tadpole
appearance.
Chondroid Syringoma: One case was noted in a 48 year old male with forehead
swelling. Histologically the epithelial cells were arranged in islands, tubules and cords
in a myxoid stroma (Fig.No.29)
Apocrine Hidrocystoma: One case was encountered in a 62year old male who
presented with a ulceroproliferative growth in external auditory canal. Interestingly
this case was associated with squamous cell carcinoma. Histologically, it showed
features of squamous cell carcinoma in some areas and other areas showed cysts lined
by columnar cells with apical snouting (Fig .No.26 )
Cylindroma: One case was noted in a 32 year old female with scalp swelling. The
tumour characteristically showed dual population of cells with jigsaw puzzle pattern
and the hyaline basement membrane showed PAS positivity (Fig. No.25).
87
Syringocystadenoma papilliferum: One case was seen over back in a 38 year old
male with epidermis showing papillomatosis and the cystic invaginations lined by two
layers of cells, the luminal cells being columnar showing apical snouting (Fig.No.28).
Sebaceous gland tumours
Sebaceous gland tumours constituted 4% of the benign adnexal tumours.
Sebaceoma: One case was noted in a 55 year old female presenting as a nodule over
nose. Histologically showed a well circumscribed mass in which more than half of the
cells were basaloid cells with few aggregates of mature sebaceous cells with extensive
keratinisation (Fig.No.33).
Malignant adnexal tumours
Adnexal carcinomas accounted for 19.4% (6 out of 31cases) of all adnexal tumours.
Table 23: Incidence of different adnexal carcinomas
Number of cases
Percentage
Hair follicle 1 16.7
Sweat gland 3 50
Sebaceous gland 2 33.3
In the present study sweat gland carcinoma was the most common type (50%)
followed by sebaceous carcinoma (33.3%) and hair follicle carcinoma (16.7%).
88
Malignant proliferating trichilemmal tumour: One case was encountered in 28
year old female who presented with an ulcer over scalp. Histologically, it showed
pleomorphic squamous cell islands with abrupt keratinisation with atypical mitotic
figures (Fig.No.34 ).
Hidradenocarcinoma: 2 cases were noted in the present study one of which was
female aged 11 years with recurrent swelling over the scalp and a male aged 45 years
with a noduloulcerative growth over abdominal wall (Fig.No.21). Histologically the
tumour cells were arranged in lobules and sheets and occasionally showed tubular
differentiation. Cells were mildly pleomorphic with clear cytoplasm (Fig.No.35).
Apocrine Carcinoma: One case was seen in a 60 year old male which occurred in
axilla (Fig.No.22). Histologically the tumours cells were atypical, arranged in sheets,
islands, tubules and singles having large pleomorphic vescicular nuclei with
prominent nucleoli and abundant eosinophilic cytoplasm with frequent atypical
mitosis.
Sebaceous carcinoma: There were 2 cases in the study presenting as swelling in the
lower eyelid in a 78 year old male and 60 year old female.
Histologically one case was well differentiated with abundant foamy
cytoplasm in all cells and another case was moderately differentiated with few areas
showing sebaceous differentiation (Fig.No.37).
89
Fig 15: Squamous cell carcinoma of foot
Fig 16: Adenoid basal cell carcinoma
Fig 17: Malignant melanoma with inguinal lymph node metastasis
90
Fig 19: Pilomatricoma
Fig 20: Proliferating trichilemmal cyst
Fig 18: Verruca vulgaris
91
Fig 21: Hidradenocarcinoma
Fig 22: Apocrine carcinoma
92
Fig 23: Seborrhoeic keratosis (40x, H&E)
Fig 24: Verrucous carcinoma (100x,H&E)
93
Fig 25: Cylindroma (100x, H&E), Inset (100x, PAS)
Fig 26: Apocrine hidrocystoma with squamous cell carcinoma (100x, H&E)
94
Fig 27: Hidradenoma (100x, H&E), Inset (400x,PAS)
Fig 28: Syringocystadenoma papilliferum (40x, H&E)
95
Fig 29: Chondroid Syringoma (100x, H&E)
Fig 30: Trichoepithelioma (100x, H&E)
96
Fig 31: Pilomatricoma (40x, H&E)
Fig 32: Proliferating trichilemmal tumour (100x, H&E)
97
Fig 33: Sebaceoma with extensive keratinisation (100x, H&E)
Fig 34: Malignant proliferating trichilemmal tumour (100x, H&E)
98
Fig 35: Hidradenocarcinoma (100x, H&E)
Fig 36: Malignant melanoma (400x, H&E)
99
Fig 37: Sebaceous carcinoma (100x, H&E)
100
DISCUSSION
Skin tumours constitute a small but significant proportion of patients with
cancer. Skin tumours are so ubiquitous that they can affect people of all ages and they
are an ideal subject for study from clinical and morphological point of view..
In this study, the WHO classification of skin tumours was followed. All the
tumours arising from mucocutaneous junction (includes tumors around the eyelids,
anterior nares, mouth, corona glandis penis, vulval orifice and the anal orifice), non
neoplastic lesions , dermal tumours and secondaries were excluded from the study.
During the 5 year study period, there was a total of 135 cases of skin tumours.
Among these, skin cancers were 89 constituting 1.3 % of total diagnosed cancers in
the Department of Pathology, KIMS, Hubli.
The ratio of benign (46) to malignant tumours(89) was 1:1.93. The ratio of
benign epidermal (11) to malignant counterpart (77) was 1:7. The ratio of benign
adnexal (25) to malignant adnexal (6) was 4.2:1. The ratio of benign melanocytic (10)
to malignant (6) counterpart was 1.6:1.
Out of 135 skin tumours, malignant epidermal tumours were most common
(57%) , followed by benign tumours of epidermal appendages (19%), benign tumours
of epidermis (8%), benign melanocytic tumours(7%) and malignant melanoma and
malignant adnexal tumours (4.5% each) .
101
Skin malignancies are rare in India compared to western countries.29 In India,
skin malignancies constitute about 1-2% of all diagnosed cancers.27
Table 24: Incidence of malignant neoplasms of skin in hospital based Indian
studies with respect to all malignant neoplasms
Hospital Author Percentage of skin
cancer
AIIMS, New Delhi Deo SV 27et al 2.4
JIPMER, Pondicherry Budharaja SN 29et al 2.08
Chittaranjan Cancer
Hospital,Calcutta Chakrvorthy RC30 et al 1.87
Government Medical
College,Jammu Kapoor R 73et al 8.16
S.R.T.R. Medical
College,Ambajogai Kulkarni PV74 et al 8
Present study 1.3
The malignant neoplasms of skin in different hospital based studies in India
ranged from 1.87% (Chakrvorthy RC30 et al) to 8.16% ( Kapoor R 73et al). It was
1.3% in the present study.
102
Table 25: Comparative incidence of different malignant tumours of skin in India
Type of tumour Bhudraja
SN29 et al.
Chakravarthy
RC30 et al
Deo SV27
et al
Present
study
Squamous cell carcinoma 49.02% 64.3% 55.8% 55%
Verrucous carcinoma - - - 9%
Basal cell carcinoma 17.65% 16.5% 18.1% 22.5%
Malignant melanoma 29.41% 8.69% 26.1% 6.7%
Adnexal carcinomas 0.98% 2.6% - 6.8%
In the present study SCC accounted for maximum number of cases (55%)
which is similar to the observations made by Chakravorthy RC30 et al, Budharaja SN
29et al ,Deo SV27 et al and Mandong BM 75et al.
In the present study the most common malignancy was SCC (55%) followed
by BCC (22.5%) , verrucous carcinoma (9%) and adnexal carcinoma (6.8%) and
malignant melanoma(6.7%).
In the study by Bhudraja SN 29et al SCC (49.02%) was the most common type
followed by malignant melanoma (29.41%), BCC (17.65%) and adnexal carcinoma
(0.98%). In the study by Chakravorthy RC30 et al SCC (64.3%) was the most common
type followed by BCC (16.5%), malignant melanoma (8.69%) and adnexal
carcinoma (2.6%) . In the study by Deo SV27 et al SCC was the most common type
(55.8%) followed by malignant melanoma (26.1%) and BCC (18.1%).
103
Benign tumours of epidermis
Verruca vulgaris: In the present study 6 cases (13%) of verruca vulgaris were
encountered. 3 cases were located on the sole of foot, 1 on leg, 1 on thigh and 1 on the
vulva. The study showed male predominance with male to female ratio of 2:1. Age
range was 10-65years. All the 6 cases showed acanthosis, hyperkeratosis,
parakeratosis and varied degree of papillomatosis. Koilocytic change was seen in 3
cases. Kilkenny M 76et al found no difference in the overall frequency of warts
between males and females.
Seborrheic keratosis: In the present study 5 cases (11%) of Seborrheic keratosis
were encountered. Age range was 38-72 years. 4 cases were located on the trunk and
one case on the ear. All the 5 (100%) cases showed acanthotic type of seborrheic
keratosis. Chen M 42et al observed 69% of cases of acanthotic type.
In the present study acanthosis was seen in all 5 cases where as hyperkeratosis,
papillomatosis, horn cysts and pigmentation were seen to a variable degree. These
findings are consistent with those of Lever et al.26
Malignant epidermal tumours
Squamous cell carcinoma
In the present study 49 cases of SCC were encountered, accounting for 55% of
all the skin malignancies. This is the commonest neoplasm in our country as
observed in the studies done by Budharaja SN 29et al, Deo SV 27et al and
Chakravorthy RC30 et al as shown in the table 25.
104
Table 26: Comparison of sex distribution in squamous cell carcinoma
Males Females
Chakravorthy RC and Dutta30 73% 27%
Budharaja SN29 et al 83% 17%
Chuang TY 77et al 60% 40%
Present study 80% 20%
In the present study, majority of the patients were males 39 patients (80%)
compared to females 10 patients (20%). This observation is similar to the studies done
by Chakravorthy RC and Dutta30, Budharaja SN 29et al and Chuang TY 77et al.
Table 27: Comparison of site distribution in squamous cell carcinoma
Budharaja
SN 29et al.
Chakravorthy
RC and Dutta30
Chuang
TY77 et al
Present
study
Head and neck 28% 21.6% 80% 24%
Trunk 12% 21.6% 6% 6%
Extremities 56% 51.4% 14% 31%
External genetalia 4%
5.4% 1% 39%
In the present study, highest number of squamous cell carcinomas (39%)
occurred over the genetalia (penis and vulva). In the study done by Chuang TY77 et al
1% of cases were noted over the penis. Chakravorthy RC and Dutta 30and Budharaja
SN29 et al included cases occurring over scrotum under external genetalia. When the
105
penile cancers are excluded, squamous cell carcinoma occurred most commonly over
the extremities in the present study, which was consistent with the findings of
Chakravorthy RC and Dutta 30 and Budharaja SN29 et al.
Verrucous carcinoma
It is a low grade variant of squamous cell carcinoma. In the present study 8
cases were encountered. Patients’ age ranged from 25 to 75years. Majority of cases
occurred in males (75%). The sites of occurrence of these tumours according to
decreasing order of frequency were foot – 4 cases (50%) , lip- 3 cases (38%) and
external genitalia-1 case (12%). These findings were similar to the observations made
by Kotwal M et al.31
Schwartz RA11et al observed foot as the most common site of occurrence. In
his study the patients’ age ranged from 23- 84 years with a male predominance (79-
89%).
Basal cell carcinoma
Table 28: Comparison of incidence of basal cell carcinoma with respect to
malignancies of skin
Percentage of basal cell
carcinoma
Budhraja SN 29et al 17.5
Chakraborthy RC and Dutta30 12
Deo SVet al27 18.10
Paymaster 29et al 30
Solanki RL33et al 28
Present study 22.5
106
In the present study the incidence of basal cell carcinoma was 22.5%. The
incidence of BCC in other studies ranged from 12% (Chakravorthy RC30 et al ) to
30% ( Paymaster29 et al)
In the present study majority of cases (85%) were seen on head and neck
which was consistent with the findings of Solanki RL33 et al (94%), Chakravorthy RC
30et al (90%) and Budhraja SN29 et al (78%).
In the present study male to female ratio was 1.2:1. Soalnki RL 33et al found a
male to female ratio of 1.26:1 and Budharaja SN29 et al found a male to female ratio
of 2.6:1
The average age was 60.6 years and peak incidence was in 8th decade in the
present study .In the study by Solanki33 et al the average age was 54 years and peak
incidence was in 5th decade .
Table 29: Comparison of histological types in basal cell carcinoma
Histological pattern of BCC Solanki RL 33et al Present study
Pigmented 6.4% 40%
Solid 60.5% 20%
Adenoid 15.7% 20%
Keratotic 9.3% 10%
Infiltrating - 5%
Basosquamous 3.5% 5%
In the present study pigmented type of BCC was most common type .In the
study by Solanki 33RL et al solid BCC was the most common type.
107
Tumours of skin appendages
There were 31 cases of appendageal tumours out of which 25 were benign and 6
malignant.
Table 30: Comparison of incidence of adnexal tumours
Benign
No %
Malignant
No %
Total No of cases
Reddy48 et al 59 69.4 26 30.6 85
Vaishnav and Dharkar48 43 89.6 5 10.4 48
Present study 25 80.6 6 19.4 31
In the present study benign tumours formed the majority (80.6%). In the study
by Vaishnav and Dharkar 48and Reddy 48et al , benign tumours formed the majority.
Benign tumours of skin appendages
There were 25 cases of benign appendageal tumours in the present study.
Table 31: Comparison of incidence of benign appendageal skin tumours
Solanki RL 79et al
Nair SP78et
al
Reddy48
et al
Kartha48 et
al
Present
study
Hair follicle
tumours
22(23.4%) 12(36.36%) 13(22%) 35(42.2%) 13(52%)
Sweat gland
tumours
50(53.2%) 19(57.56%) 43(73%) 45(54.2%) 11(44%)
Sebaceous
gland tumours
22(23.4%) 2(6.06%) 3(5%) 3(3.6%) 1(4%)
Total No of
cases
94 33 59 83 25
108
The occurrence of hair follicle tumours (52%) was higher in the present study.
The occurrence of sweat gland tumours was higher in the studies done by Solanki
RL79 et (53.2%) , Nair SP78 et al (57.56%) and Kartha48 et al (54.2%)
Tumours of hair follicle differentiation
In the present study there were 13 patients with tumours of hair follicle
differentiation accounting for 52% of all the benign appendageal tumours. There was
female preponderance with the female to male ratio of 3.33:1. This finding was
similar to the study of Marrogi AJ 80et al with female to male ratio of 6:1.
Table 32: Comparison of incidence of benign hair follicle tumours
Solanki RL20 et
al
Reddy48 et
al
Kartha48 et al Present
study
Pilomatricoma 15(68.18%) 9(69%) 20(57.14%) 4(31%)
Trichoepithelioma 5(22.72%) 4(31%) 13(37.15%) 2(15%)
Trichilemmoma 2(9.09%) - - -
Proliferating
trichilemmal tumour
- - - 7(54%)
Trichofolliculoma - - 2(5.7%) -
Total No of cases 22 13 35 13
The occurrence of proliferating trichilemmal tumour (54%) is higher in the
present study followed by pilomatricoma (31%) and trichoepithelioma (15%) .
In the study by Solanki RL20 et al, Kartha48 et al and Reddy48 et al the
occurrence of pilomatricoma was higher followed by trichoepithelioma.
Trichilemmoma occured in the study by Solanki RL20 et al and
trichofolliculoma occured in the study by Kartha48 et al.
109
Proliferating trichilemmal tumour: There were 7 cases in the present study
accounting for 54% of the benign tumours of hair follicle. Histologically, the lesion
showed a well defined tumour composed of squamous cells showing abrupt
keratinisation. Presence of calcification, pleomorphism of tumour cells, dyskeratosis
and squamous eddies were noted. These observations were similar to those of Prakash
kumar55 et al and Headington JT47.
Proliferating trichilemmal tumour is believed to originate from a pre-existing
pilar cyst.49 There was one case of proliferating trichilemmal tumour in a 60 year old
male with scalp swelling which had developed inside a pilar cyst.
Pilomatricoma : 4 cases were noted in the present study accounting for 31% of the
benign tumours, with male to female ratio of 1:3 and mean age at presentation was 27
years. In the study by Solanki RL20 et al the male to female ratio was 1:1 and mean
age was 28 years. Histologically the tumours were well circumscribed ,composed of
islands of basophilic cells and shadow cells. Calcification and giant cell reaction to
keratin was also noted. These observations were similar to those of Solanki RL20 et al.
Trichoepithelioma: Two cases were encountered in the study accounting for 15% of
the benign tumours. Both were females aged 50 and 80 years. Both the lesions were
located over the face. Histologically, they showed islands of basaloid cells in the
dermis with peripheral palisading of cells. Horn cysts and presence of fibrous stroma
was noted. These observations were similar to those of Alsaad KO49 et al and Solanki
RL20et al.
110
Tumours of sweat gland differentiation
There were 11 patients with sweat gland differentiation accounting for 44% of
the benign adnexal tumours.
Table 33: Comparison of incidence of benign tumours of sweat gland
Tumours Solanki RL79
et al
Reddy 48et
al
Nair SP78 et
al
Present
study
Hidradenoma 13(27.6%) 29(67.4%) 1(5.3%) 6(55%)
Cylindroma 3(6.4%) 1(2.3%) 1(5.3%) 1(9%)
Chondroid syringoma 11(23.4%) 2(4.6%) - 1(9%)
Apocrine
hidrocystoma
- - - 1(9%)
Syringoma - 3(7%) 14(73.7%) 1(9%)
Spiradenoma 5(10.6%) 2(4.6%) 2(10.5) -
Syringocystadenoma
papilliferum
11(23.4%) 3(7%) 1(5.3%) 1(9%)
Hidradenoma
papilliferum
2(4.3%) - - -
Eccrine poroma 2(4.3%) - - -
Unclassified - 39(7%) - -
Total No of cases 47 43 19 11
The occurrence of hidradenoma (55%) was higher in the present study
followed by 9% each of syringoma, chondroid syringoma, cylindroma, apocrine
hidrocystoma and syringocystadenoma papilliferum.
In the study by Solanki RL79 et al hidradenoma (27.6%) was the most common
followed by 23.4% each of chondroid syringoma and syringocystadenoma
papilliferum.
111
In the study by Nair SP 48et al syringoma (73.7%) was the most common
tumour.
In the study by Reddy 48et al hidradenoma(67.4%) was the most common
tumour.
Hidradenoma: 6 cases were encountered in the study accounting for 55% of sweat
gland tumours, out of which 4 were females and 2 males with male to female ratio of
1:2. Four cases were seen on the trunk and 2 on the face.
In the study by Solanki RL79 et al hidradenoma accounted for 27.6% (13
cases) of sweat gland tumours of which 7 were males and 6 females with a male to
female ratio of 1.16:1.
Syringoma: One case of syringoma was noted in 27 year old female over eye lid.
Histologically the epithelial cells were arranged in nests and tubules showing tadpole
appearance. Similar observations have been made by Berke A17 et al.
Chondroid Syringoma: One case was noted in the present study accounting for 9%
of sweat gland tumours, in a 48 year old male with forehead swelling. Solanki RL79 et
al encountered 11 cases of chondroid syringoma accounting for 23.4% of sweat gland
tumours with male to female ratio of 1.75:1.
Histologically the epithelial cells were arranged in islands, tubules and cords
in a myxoid stroma. Similar observations have been made by Berke A 17et al.
112
Apocrine Hidrocystoma: One case of unusual combination of apocrine
hidrocystoma with squamous cell carcinoma was encountered in a 62year old male
located in the external auditory canal.
Cylindroma: One case was noted in a 32 year old female with scalp swelling. The
tumour characteristically showed dual population of cells arranged in jigsaw puzzle
pattern. Solanki RL79 et al observed all the 3 cases in males. Scalp is the most
common site for cylindroma as observed by Berke A 17et al.
Syringocystadenoma papilliferum: One case was encountered in the present study
accounting for 9% of sweat gland tumours, in a 38 year old male over back.
Solanki RL 79et al reported 11 cases accounting for 23.4% of sweat gland
tumours of which 4 were males and 7 females. Majority of cases occurred over head
and neck (64%) followed by 18% each over trunk and thigh.
Tumours of sebaceous differentiation
Sebaceoma: One case was noted in a 55 year old female presenting as a nodule over
nose accounting for 4% of benign adnexal tumours. Histologically, it showed a well
circumscribed mass in which more than half of the cells were basaloid with few
aggregates of mature sebaceous cells. These observations were similar to that of
Lever 7et al and Weedon D5 et al.
Adnexal carcinoma
In the present study adnexal carcinomas accounted for 19.4% (6 out of
31cases) of all adnexal tumours. In the study by Reddy 48et al adnexal carcinomas
113
accounted for 30.6% (26 out of 85 cases) of adnexal tumours. In the study by
Vaishnav and Dharkar 48adnexal carcinomas accounted for 10.4% (5 out of 48 cases)
of adnexal tumours as shown in table 30.
Table 34: Comparison of incidence of different adnexal carcinomas
Reddy 48et al
No %
Vaishnav and Dharkar48
No %
Present study
No %
Hair follicle - - - - 1 16.7
Sweat gland 11 42.3 5 100 3 50
Sebaceous 15 57.7 - - 2 33.3
Total 26 100 5 100 6 100
In the present study sweat gland carcinoma was the most common type (50%)
followed by sebaceous carcinoma (33.3%) and hair follicle carcinoma (16.7%).
In the study by Reddy48 et al sebaceous carcinoma was the most common type
(57.7%) followed by sweat gland carcinoma (42.3%). In the study by Vaishnav and
Dharkar 48all the cases (100%) were of sweat gland carcinoma.
Malignant proliferating trichilemmal tumour: One case was encountered in 28
year old female who presented with an ulcer over scalp accounting for 16.7% of
adnexal carcinomas. Histologically it showed pleomorphic squamous cell islands with
abrupt keratinisation with atypical mitotic figures. Similar observations have been
made by Mehregan AH7 et al.
114
Sweat gland carcinoma
In the present study 3 cases were encountered, 2 males and 1 female with male
to female ratio of 2:1. The age range was 11-60 years.
In the study by Solanki RL79 et al 3 cases were encountered with male to
female ratio of 2:1.The age range was 44-70 years. Reddy et al has reported a male to
female ratio of 1:1.27 and the age range was 8-70 years with maximum cases in 4th to
6th decade.
Hidradenocarcinoma: 2 cases were noted in the present study one of which was
female aged 11 years and a male aged 45 years. Histologically the tumour cells were
arranged in lobules and sheets and occasionally showed tubular differentiation. Cells
were mildly pleomorphic with clear cytoplasm. Similar observations have been made
by Gauerke S81 et al.
Apocrine carcinoma: The present study observed one rare case of apocrine
carcinoma in the axilla of a 60 year old male. Similarly Reddy et al encountered one
case of apocrine carcinoma.
Sebaceous carcinoma: There were 2 cases in the present study accounting for 33.3%
of adnexal carcinomas both located in the eyelid of a 78 year old male and 60 year old
female with male to female ratio of 1:1.
Reddy 48et al has encountered 15 cases accounting for 57.7% of adnexal
carcinomas with male to female ratio of 2:1 and 33.3% of cases were located in
eyelid. In the present study 100% of cases are located in eyelid.
115
Tumours of melanocytic system
Benign melanocytic nevus: In this study 10 cases were seen among which 9 were
intadermal and 1 was compound nevus. All 10 cases were seen in head and neck
region. Peak incidence was seen between 20-40 years (60%). Shoko M 82et al has
analysed 531 cases of nevus out of which 15 were junctional, 134 cases were
compound, and 382 cases were dermal.
Histologically the dermis showed nests, cords and sheets of nevus cells
showing maturation; junctional activity was seen in 1 case.
Malignant Melanoma
Table 35: Comparison of incidence of malignant melanoma
Incidence of malignant melanoma
Chakravorthy and Dutta30 8.69%
Deo SV 27et L 26.1%
Paymaster 29et al 8.7%
Budharaja 29et al 29.4%
Chitkara 29et al 7%
Present study 6.7%
In Indian studies malignant melanoma accounted for 7% to 29.4% of all skin
cancers. In the present study it accounted for 6.7%.
116
Table 36: Comparison of sex incidence of malignant melanoma
Male Female
Sampat and Sirsut71 71.8% 28.2%
Chakravorthy and Dutta30 80% 20%
Mukhopadhyay S83 et al 82% 18%
Katalinic A 84et al 56.7% 43.3%
Present study 83% 17%
In the present study incidence of malignant melanoma was more in males
which was consistent with the findings of Sampat and Sirsut71, Chakravorthy and
Dutta30, Mukhopadhyay S83 et al and Katalinic A 84et al.
Table 37: Comparison of age incidence of malignant melanoma
Age in years Katalinic A84 et
al
Mukhopadhyay S83 et
al
Present study
0-19 1.2% - -
20-39 21.4% 18.2% 16.66%
40-59 31.4% 27.3% 16.66%
60-79 38.8% 45.5% 66.66%
80+ 7.3% 9% -
In the present study majority of cases (66.66%) occurred in the age range of
60-79 years. Similar observations were made by Katalinic A 84et al (38.8%) and
Mukhopadhyay S 83et al (45.5%).
117
Table 38: Comparison of site distribution of malignant melanoma
Site Sampat and
Sirsut71
Chatkara 29et al
Mukhopadhyay
S 83et al
Present
study
Head and neck 13% 20% 10% 16.7%
Trunk 5% - 10% -
Extremities 82% 80% 80% 83.3%
Total No of cases 74 10 10 6
In the present study majority of cases (83.3%) were located over extremities.
Similar observations were done by Sampat and Sirsut71, Mukhopadhyay S83 et al and
Chitkara 29et al.
Table 39: Comparison of location of malignant melanoma over foot
Foot
Sampat and Sirsut71 54%
Budharaja SN 29et al 83%
Chakravorthy and Dutta30 80%
Present study 83%
In the present study majority of cases 83% (5 cases) were seen on the foot.
Similar observations were done by Sampat and Sirsut71, Budharaja SN 29et al and
Chakravorthy and Dutta30.
118
Table 40: Comparison of Clark’s grading of malignant melanoma
Mukhopadhyay S71 et al
No %
Present study
No %
Grade 1 2 18.2 0
Grade 2 2 18.2 0
Grade 3 4 36.4 1 17
Grade 4 2 18.2 5 83
Grade 5 1 9 0
Total No of cases 11 6
In the present study 83% of cases were grade 4 and 17% of cases were grade
3. In the study by Mukhopadhyay S 71et al majority of cases were grade 3 (36.4%),
followed by 18.2% each of grade 1, grade 2 and grade 4 and 9% of grade 5.
119
CONCLUSION
Skin tumours constitute a small but significant proportion of patients with
cancer. The skin is a complex organ. Because of its complexity a wide range of
diseases can develop from the skin including tumors from surface epidermis,
epidermal appendages and dermal tissue.
The diagnosis of skin tumours presents unique difficulties, in part, related to
the wide variety of tumors and the complicated nomenclature. The study of
histogenesis of the adnexal tumours is interesting, fascinating and challenging
because of wide range of differentiation.
Unlike in the Western countries, SCC is the commonest malignant skin
tumour in India. Histopathological study is one of the most valuable means of
diagnosis in dermatopathology and the diagnosis of skin tumours can be done by
correlating clinical features, gross and histological appearances.
The present study emphasizes the various patterns of skin neoplasms in this
geographic location in and around Hubli.
Finally the quintescence of the subject of study of skin tumours is it’s
vastness, it’s enormity and its interesting histomorphology.
120
SUMMARY
1. Skin tumours constitute a small but significant proportion of patients with cancer.
Skin tumours are an ideal subject for study from clinical and morphological point
of view and so ubiquitous that they can affect people of all ages.
2. A histopathological study of 135 cases of skin tumours ( this includes tumours of
epidermis, melanocytes and skin appendages ) was carried out in Department of
Pathology , Karnataka Institute Of Medical Sciences, Hubli over a period of 5
years.
3. Out of 135 cases, 46 were diagnosed as benign and 89 as malignant tumours of
skin constituting 34% and 66% respectively.
4. The ratio of malignant to benign tumours was 1.93: 1 with male to female ratio
of 1.57: 1.
5. Out of a total 6,803 cancers detected in the Department of Pathology, 89 cases of
skin malignancies were encountered which accounted for 1.3% of all diagnosed
cancers.
6. Among the 46 benign tumours, 25(54%) were tumours of skin appendages, 11
(24%) were epidermal in origin and 10 (22%) were from melanocytic origin.
7. Out of 89 malignant tumours, 77 (86.5%) were tumours of epidermal origin, 6
(6.8%) were of skin appendages and 6 (6.7%) were from the melanocytic origin.
8. Of the benign epidermal tumours, 6 (55%) were verruca vulgaris and 5 (45%)
were seborrheic keratosis.
9. 77 cases of malignant epidermal tumours were encountered, of which squamous
cell carcinoma was commonest (49 cases-64%), followed by basal cell carcinoma
(20 cases -26%) and Verrucous carcinoma (8 cases-10%).
121
10. 49 cases of SCC were encountered accounting for 55% of all the malignant
neoplasms of skin with peak incidence in 7th decade in males and 6th decade in
females with male preponderance (80%) and maximum number of cases (39%)
occurred in external genetalia (penis) in males and head and neck and extremities
in females. Majority of the squamous cell carcinomas were well differentiated (
71%).
11. 8 cases of verrucous carcinoma were encountered. Patients’ age ranged from 25
to 75 years. Majority of cases occurred in males (75%) with male to female ratio
of 3:1. The sites of occurrence of these tumours according to decreasing order of
frequency were foot – 4 cases, lip- 3 cases and external genitalia-1 case.
12. 20 cases of basal cell carcinoma were encountered accounting for 22.5% of all the
malignant neoplasms of skin. Peak incidence was in 8th decade with male
preponderance with male to female ratio of 1.2: 1. Mean age of patients was 60.6
years. 85% of cases were located on head and neck and majority of these were
seen in the eye lid.
13. In the present study 31 cases of skin adnexal tumours were encountered, out of
which 25 were benign and 6 were malignant. Benign tumours formed the majority
(80.6%)
14. Among the benign adnexal tumours the occurrence of hair follicle tumours (13
cases-52%) was higher in the present study followed by sweat gland tumours (11
cases-44%) and sebaceous tumours (1 case-4%).
15. Hair follicle tumours constituted 52% of the benign adnexal tumours out of which
majority (7 cases-54%) of cases were proliferating trichilemmal tumour followed
by pilomatricoma (4 cases-31%), trichoepithelioma (2 cases-15%) .Majority of
cases were seen in females with male to female ratio of 1:3.33.
122
16. Sweat gland tumours constituted 44% of benign adnexal tumours out of which
(6cases) 55% of cases were of hidradenoma followed by (1 case) 9% each of
syringoma, chondroid syringoma, cylindroma, apocrine hidrocystoma,
syringocystadenoma papilliferum and apocrine carcinoma. The male to female
ratio was 1:1.2.
17. Sebaceous gland tumours constituted 4% of the benign adnexal tumours. Only one
case of sebaceoma was noted.
18. Among the malignant adnexal tumours sweat gland carcinoma was the most
common type (3 cases -50%) followed by sebaceous carcinoma (2 cases -33.3%)
and hair follicle carcinoma (1 case- 16.7%).
19. 3 cases of sweat gland carcinoma were encountered among which 2 were
hidradenocarcinoma and 1 apocrine carcinoma. There were seen in 2 males and 1
female with male to female ratio of 2:1. The age ranged from 11-60 years.
20. 16 cases of tumours of melanocytic origin were encountered, of which 10 (62.5%)
were nevocellular nevus and 6 (37.5%) were malignant melanoma.
21. 6 cases of malignant melanoma were encountered accounting for 6.7% of all
malignant skin tumours. The youngest age was 28 years and oldest age was 70
years. Majority of cases were between 60-79 years (66.66%). Sex distribution
showed a significant difference with 83% males and 17% females showing male
predominance. The most common site was sole (5 cases) and one case occurred in
ear lobe. 83% of cases showed infiltration upto reticular dermis (Clark’s grade 4).
Metastatic spread to lymph nodes was seen in 2 cases.
123
REFERENCES
1. Murphy GF, Sellheyer K and Mihm MC. The skin. In Robbins and Cotran
Pathological basis of disease. 7th ed. Philadelphia : Saunders; 2008.p.1227-1271.
2. Koh D, Wang H, Lee J, Chia KS, Lee HP and Goh CL. Basal cell carcinoma,
squamous cell carcinoma and melanoma of the skin: analysis of the Singapore
Cancer Registry data 1968-97. British journal of Dermatology; 148:1161-1166.
3. LeBoit PE, Burg G, Weedon D and Sarasin A. Pathology and genetics of skin
tumours. In World health organisation classification of tumours. IARC press.
Lyon, 2006.p.9-164.
4. Elder DE, Elenitsas R. Benign pigmented lesions and malignant melanoma. In
Lever’s histopathology of skin. 9th ed. Philadelphia: Lippincott Raven; 2005. p.
715-804.
5. David W. Tumors of cutaneous appendages. In: Weedon David’s Skin Pathology.
Churchill Livingstone; 2002. p. 859-916.
6. Reddy MK., Veliath AJ, Nagarajan S and Aurora AL. A clinicopathological study
of adnexal tumours of skin. Indian journal of medical research, june 1982:p. 882-
889.
7. Klein W, Chan E and Seykora JT. Tumours of the epidermal appendages. In In
Lever’s histopathology of skin. 9th ed. Philadelphia: Lippincott Raven; 2005.
p.867-926.
8. Emmet AJJ and O’Rourke MGE. Malignant skin tumours. Churchill livingstone,
1982 :p1-478.
9. Freedburg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LD and Katz SI.
Fitzpatrick’s dermatology in general medicine, McGraw-Hill; 6th ed. 2003.p
11123456678990-
124
10. Schwartz RA. Keratoacanthoma Continuing medical education. J Am Acad of
Dermatol; Jan 1994;30(1):1-17.
11. Schwartz RA. Verrucous carcinoma of skin and mucosa Continuing medical
education. J Am Acad of Dermatol ;Jan 1995 ;32(1):1-15.
12. Weedon D. Lentigenes, nevi and melanomas. In: Weedon David’s Skin
Pathology. 2nd ed.Churchill Livingstone; 2002. p. 803-835.
13. Kapadia RD and Chatura KR. Malignant pilomatricoma. Indian journal of
Dermatology Verereol Leprology; 1990; 56:450-451.
14. Lapansri S and Mihm CM. Pilomatrix carcinoma or calcifying epitheliocarcinoma
of Malherbe. Cancer 45; 1980: 2368-2373.
15. Nelson BR, Hamlet RK, Gillard M, Railan and Johnson TM. Sebaceous
carcinoma- continuing medical education. American Academy of Dermatology,
vol 33, No.1; 1995:1-9.
16. Headington JT . Mixed tumours of skin: Eccrine and Apocrine types. Archives of
Dermatology, vol.84; 1961:151-158.
17. Berke A and Kels JMG. Eccrine sweat gland disorders. Part 1- Neoplasms.
International Journal of Dermatology, vol.33, No.2, 1994:79-85.
18. McCalmont, Timothy H; Eight insights into the interrelationship of adnexal
neoplasms, The Amerian journal of Dermatopathology, April 1996; 18(2):1-12.
19. Hunt SJ, Kilzer PB and Santa Cruz DJ. Desmoplastic trichilemmoma: histologic
varient resembling invasive carcinoma. Journal of cutaneous pathology ;
1990:17:45-52.
20. Solanki RL., Anand VK, Gaur SK, Arora HL and Gupta R . Neoplasms of hair
follicle. Indian journal of Dermatology Verereol Leprology; 1989;55:33-37.
125
21. Ackerman BA et al. Embryologic, histologic and anatomical aspects. Histologic
diagnosis of inflammatory skin diseases, 2nd edi,p 3-56.
22. Singh I. Human embryology. 7th ed. McMillan; 2003: p. 103-109.
23. Murphy GF. Histology of skin: In Lever’s histopathology of skin. 9th ed.
Philadelphia: Lippincott Raven; 2005. p.9-58.
24. Young B, Lowe JS, Stevens A and Heath JW. Skin. In Wheater’s functional
histology. 5th ed.Churchill livingstone;2006. p.167-185.
25. Singh I. Skin and its appendages. In: Textbook of Human Histology.4th ed.
Jaypee; 2002. p. 193-206.
26. Kirkham N. Tumours and cysts of epidermis. In Lever’s histopathology of skin.
9th ed. Philadelphia: Lippincott Raven; 2005. p.805-866.
27. Deo SV. Surgical management of skin cancers: Experience from a regional cancer
centre in North India. Indian Journal of Cancer 2005; 42:145-50.
28. Mckee PH and Brenn T .Tumours of surface epithelium. In pathology of skin.
Elsevier Mosby, 3rd ed; p1153-1237.
29. Budharaja SN, Pillai VCV, Periyanagam WJ, Kaushik SP and Bedi BMS.
Malignant neoplasms of skin in Pondicherry- a study of 102 cases. The Indian
Journal of Cancer,1972: 284-295.
30. Charkravorthy RC and Choudhuri DR. Malignant neoplasms of the skin in Eastern
India. The Indian Journal of Cancer, vol 5,1968:133-144.
31. Kotwal M, Poflee S and Sudhakar B. Carcinoma cuniculatum at various
anatomical sites. Indian J Dermatol; 50; 2005:216-20.
32. Kikuchi A, Shimizu H and Nishikawa T, Clinical and histopathological
characteristics of basal cell carcinoma in Japanese patients, Arch
Dermatol.1996;132:320-324.
126
33. Solanki RL, Arora HL, Anand VK, Gaur SK, Gupta R. Basal cell epithelioma ( A
clinicopathological study of 172 cases), Indian J Dermatol Venerol Leprol
;1989(55):33-43.
34. Rahbari H and Mehregan AH. Basal cell epithelioma in children and teenagers.
Cancer 49;1982: 350-353.
35. Requena L, Martin L, Farina MC, Pique E and Escalonilla P. Keloidal basal cell
carcinoma: A new clinicopathological variant of basal cell carcinoma. Br J
Dermatol; 1996(134):953-957.
36. Scrivener Y, Grosshans and Cribier B. Variations of BCC according to gender,
age, location and histological type. British journal of Dermatology 2002: 147:41-
47.
37. Leffell DJ, Headington JT et al. Aggressive growth basal cell carcinoma in young
adults. Arch Dermatol, 127; 1991:1663-1667.
38. Johnson SC and Bennet RG, Occurrence of basal cell carcinoma among multiple
trichoepitheliomas, Journal of American Academy of Dermatology 1993; 28:322-
326.
39. Hendrix JD and Parlette. Micronodular basal cell carcinoma. Arch Dermatol, vol
132;1996:295-298.
40. Marks R, Rennie G and Selwood T. The relationship of basal cell carcinomas and
squamous cell carcinomas to solar keratosis. Arch Dermatol 1988;124:1039-1042.
41. David W. Tumors of the epidermis. In: Weedon David’s Skin Pathology.2nd ed.
Churchill Livingstone; 2002. p. 754-82.
42. Chen M, Shinmori H, Takemiya M, Milki Y. Acantholytic variant of seborrheic
keratosis. J Cutan Pathol, 1990;17:27-31.
127
43. Maize JC and Sinder RL. Non melanoma skin cancer in association with
seborrheic keratosis: Clinicopathologic correlations. Dermatol Surg 21; 1995:
960-962.
44. Kingman J and Callen JP. Keratoacanthoma, a clinical study. Archives of
dermatology; June 1984; vol 120:p.736-740.
45. Cooper PH and Wolfe JT. Perioral Keratoacanthomas with extensive perineural
invasion and intravenous growth. Archives of dermatology; Sept 1988; vol
124:p.1397-1401.
46. Chandrashekaran CV, Raghuveer CV and Prakash S. Epidermal cysts - a
clinicopathological and biochemical study. Postgradutate Medical Journal;
December 1980; 56: 823-827.
47. Headington J.T. Tumours of the hair follicle. Amerian journal of pathology; Nov
1976; 85(2): 480-501.
48. Reddy KM, Veliath AJ, Nagarajan S and Arora AL. A clinicapathological study
of adnexal tumours of skin. Indian J Med Res 75, June 1982:882-889.
49. Alsaad KO, Obaidat NA, Ghazarian D. Skin adnexal neoplasms. Part 1. An
approach to tumors of the pilosebaceous unit. Journal of Clinical Pathology 2007;
129-144.
50. Hashimoto K and Lever WF. Histogenesis of skin appendage tumors. Archives of
Dermatology, vol 100, Sept 1969: 356-370.
51. Shapiro PE and Kopf AW. Familial multiple desmpolastic trichoepitheliomas .
Archives of Dermatology; 1991; 127:83-87.
52. Beck S and Cotton DWK. Recurrent solitary giant trichoepithelioma located in the
perianal area; a case report. British journal of Dermatology; 1988, p.563-566.
128
53. Brownstein HM and Shapiro L. Desmoplastic trichoepithelioma. Cancer
40;1977:2979-2986.
54. Thomas JA and Kothare SN. Calcifying epithelioma of Malherbe- A true tumour
or a malformation. The Indian journal of cancer; June 1975:179-186.
55. Kumar P, Chatura KR, Haravi MR and Chandrashekar HR. Proliferating
trichilemmal cyst mimicking squamous cell carcinoma . Indian journal of
Dermatology, Verereology and Leprology, 2000; 66: 149-50.
56. Brownstein H.M and Shapiro L. Trichilemmoma- Analysis of 40 cases. Archives
of Dermatology; vol 107; June 1973:866-869.
57. Reis JP, Tellechea O, Cunha MF and Baptista A.P. Trichilemmal carcinoma :
review of 8 cases. Journal of Cutaneous Pathology; 1993; 20: 44-49.
58. Rulon DB and Helwig EB. Cutaneous sebaceous neoplasms. Cancer, vol 3, 1974:
82-102.
59. Sulica RL, Kao GF and Penneys NS. Eccrine angiomatous harmartoma. Journal of
cutaneous pathology 1994:21:71-75.
60. Amin SP and Shah BH. Syringoma- a case report with review of literature. Indian
journal of Dermatology, Venereology and Leprology, vol39, No 3;1973:133-137.
61. Rongioletti, Semino MT and Rebora A. Unilateral multiple plauque like
syringoma. British journal of Dermatology 1996; 135:623-625.
62. Evans HL, Daniel SP, Smith JL and Winkelman RK. Carcinoma arising in eccrine
spiradenoma. Cancer 43, 1979: 1881-1884.
63. Ishimura E, Iwamoto H, Kobashi Y, Yambe H and Ichijima K. Malignant
chondroid syringoma. Cancer 52; 1983: 1966-1973.
64. Stephen MAJ, Rosten MC, Jack MAJ. Syringocystadenoma papilliferum in an
unusual location. Arch Dermatol, vol 112, June 1976:pp1274-1281
129
65. Mammino JJ and Vidmar DA. Syringocystadenoma papilliferum. International
Journal of Dermatology, vol 30; 11; 1991:835-836.
66. Kumar V, Garg BR, Baruah MC and Ratnakar C. Syringocystadenoma
papilliferum. Indian journal of Dermatology, Verereology and Leprology,
1991:57:150-151.
67. Marghoob AA, Schenbach SP, Kopf AW, Orlow SJ, Nossa R and Bart RS. Large
congenital melanocytic nevi and the risk for the development of malignant
melanoma-a prospective study. Arch Dermatol, vol 132, 1996:170-175.
68. Illig L, Weidner F, Hundeiker M, Gartmann H, Biess B, Leyh F and Paul E.
Congenital nevi <10 cm as precursors to melanoma, 52 cases, a review and a
conception. Arch Dermatol, vol 121, october 1985:pp1274-1281.
69. Murphy GF and Mihm MC. Recognition and evaluation of cytological dysplasia
in acquired melanocytic nevi. Human Pathology, vol 30, No.5; 1999: 506-511.
70. Blessing K. Benign atypical nevi: diagnostic difficulties and continued
controversy. Histopathology 34, 189-198.
71. Sampat MB, Sirsat MV. Malignant melanoma of the skin and mucous membranes
in Indians. Ind J Cancer 1966; 6: 228-53.
72. Banerjee SS and Harris M. Morphological and immunophenotypic variations in
malignant melanoma.Histopathology 2000, 36: 387-402.
73. Kapoor R, Goswami KC. Pattern of cancer in Jammu region (Hospital based study
1978-89). Ind J Cancer 1993; 30:67-71.
74. Kulkarni PV, Jaiswal SS. Profile of malignancies at medical college. Ambojogai
(15 years retrospective study). Ind J Cancer 1996; 33:31-6.
130
75. Mondong BM, Orkar KS, Sule AZ and Dakum NL. Malignant skin tumours in Jos
university teaching hospital, Jos, Nigeria (Hospital based study). The Nigerian
Journal of Surgical Research, vol 3, No. 1. March 2001:234-238.
76. Kilkenny et al. The prevalence of common skin conditions in Australian school
students: 1. Common, plane and plantar viral warts. Br J Dermatol. 1998 May;138
(5):840-5.
77. Chuang TY, Popescu AP. Squamous cell carcinoma. A population based
incidence study in Rochoster,Minn. Arch Dermatol 1990;126:185-8.
78. Nair SP. A clinicopathological study of skin appendageal tumours. Indian J of
Dermatol Venerol Leprol 200874:108-550
79. Solanki RL, Anand VK. Neoplasms of sweat gland. Indian J of Dermatol Venerol
Leprol 1989; 55:108-112.
80. Marrogi A.J, Wick M.R and Dehner L.P, Benign cutaneous adnexal tumors in
childhood and young adults, excluding pilomatricoma: review of 28 cases and
literature. Journal of cutaneous pathology 1991: 18:20-27.
81. Gauerke S and Driscoll JJ. Hidradenocarcinomas – a brief review and future
directions. Arch Pathol Lab Med, vol 134, May 2010:781-785.
82. Shoko M. The histopathological analysis of 531 cases of melanocytic nevus of
the face. Japanese Journal of Dermatology 2002; vol.112;No.6: 803-810.
83. Mukhopadhyay S et al. A clinicopathological study of malignant melanoma with
special reference to atypical presentation. Indian Journal of Pathology and
Microbiology, 51(4); Oct-Dec 2008:485-488.
84. Katalinic A. Epidemiology of cutaneous melanoma and non-melanoma skin
cancer in Schleswig- Holstein, Germany: incidence, clinical subtypes, tumour
stages and localization. British Journal of Dermatology.2003:149:1200-1206.
131
PROFORMA
HISTOPATHOLOGICAL STUDY OF SKIN TUMOURS DEPARTMENT OF PATHOLOGY, KIMS, HUBLI.
GUIDE: Study done by:
Dr. Rekha B Puranik Dr. Sonam S. Shaikh
• SERIAL NO:
• BIOPSY NO:
1) Particulars of patient:
Name-
Age-
Sex-
IP/OP No.-
Ward/ Unit-
2) Clinical findings:
o Single / multiple
o Site of lesion-
o Duration of symptoms-
o Presenting symptoms- Non healing ulcer / Swelling / Nodule / Papule
/Ulceroproliferative / Noduloulcerative / Fungating / Sinus / Wart /
Verrucous / Pigmented / Crateriform / mole
o Consistency – Soft / Cystic / Firm / Hard
o Pruritus – Present / Absent
o Bleeds on touch –Present / Absent
o Past history – Similar complaints / Others
132
3) Type of surgical specimen:
o Punch Biopsy / Wedge Biopsy / Excision Biopsy / Amputation /
Shave biopsy / Wide local excision / Lymph node dissection
4) Histopathological examination:
Gross :
No. of bits:
Size of largest bit of tissue:
Size of the lesion:
Colour of the lesion:
External Surface : Flat / Elevated / Ulcerated/ Ulceroproliferative
growth / Verrucous lesion / Pigmented / Globular mass / Smooth
surface / Ruptured cyst wall
Consistency – Soft / Firm / Hard:
Cut Section: solid/ cystic
Tumour location & relation of lesion to skin & underlying
structures:
Contents of cyst: pultaceous material / Hair
Margins of the Specimen:
Microscopy:
A) Location of tumour:
Intra-epidermal/ Junctional / Intradermal / Subcutaneous / Full thickness
B) Tumour origin:
a. Epidermal
b. Adnexal:
Hair Follicle Differentiation
133
Sebaceous Differentiation
Apocrine Differentiation
Eccrine Differentiation
c. Melanocytic
C) Circumscription: Well / Poorly / Infiltrative / Pushing
D) Cystic lesions:
I. Wall : Epidermal / Others
II. Granular Layer: Present / Absent
III. Appendages: Present / Absent – Hair Follicle, Sebaceous, Eccrine,
Apocrine
IV. Content: Laminated Keratin / Homogenous Eosinophilic Material
/Others
V. Intercellular Bridges : Clearly Visible / Not visible
VI. Palisading of Cells: Present / Absent
VII. Swollen Cells: Present / Absent
E) Epidermis:
Unremarkable / Hyperkeratosis / Parakeratosis / Acanthosis / Papillomatosis/
Invaginations / Elongated Rete Ridges / Bulbous Downward Proliferation
/Spinous Proliferation / Ulcerated /Thinned out /Koilocytic change / Absent /
Pigment seen
F) Keratinisation:
• Epidermal Keratinisation
• Trichilemmal Keratinisation
• Horn Cysts
• Pseudohorn Cysts
134
• Keratin Pearls – Present – Many /Few / Occasional
• Dyskeratosis - Present – Many /Few / Absent
G) Dermis : Unremarkable / Involved
H) Adnexa : Hair Follicle – Tumor/ Present / Absent / UR
Sebaceous Glands – Tumor /Present / Absent / UR
Sweat Glands- Tumor /Present / Absent / UR
I) Tumour connection to epidermis: Present / Absent
J) Tumour cells :
i. Squamous cells
ii. Basaloid cells
iii. Melanocytic cells – Nevus cells / Melanoma cells
iv. Sebaceous cells
v. Shadow / ghost cells
vi. Basophilic cells
vii. Glandular /Ductal epithelial cells – Cuboidal, Columnar , Flattened
viii. Clear cells
ix. Undifferentiated
K) Cell arrangement:
• Irregular mass / Sheets / Islands / Nests / Tubular / Lobules /
Columns / Cords / Bands / lacelike / Singles / Cystic / Trabecular /
Papillary /Fascicular / Peripheral Palisading / Ductal differencition
/ Clefting artifact / Squamous eddies / Intercellular bridges /
Hyaline material / Jigsaw puzzle / Tadpole appearance / Junctional
activity.
135
L) Cells :
• Uniform / Biphasic / Triphasic / Pleomorphic
M) Cell shape:
• Polygonal / Round / Oval / Spindle / Columnar / Cuboidal
N) Nucleus :
i. Small / Large / Round / Oval / Central / Eccentric / Monomorphic /
Mildly pleomorphic / Pleomorphic
ii. Chromatin pattern – Normochromatic / Hyperchromatic / Finely
distributed / Coarsely distributed / Vescicular / Stippled
iii. Nucleoli – prominent – Eosinophilic / Basophilic
- Inconspicuous / Absent
O) Cytoplasm:
• Amount - Scanty / Moderate / Abundant
• Quality - Eosinophilic / Basophilic / Clear / Foamy / Granular /
Melanin granules / Apical Snouts
P) Cell borders : Distinct / Indistinct
Q) Secretions : Present / Absent
R) Stroma :
o Unremarkable / Loose / Dense / Fibroblastic / Myxoid /
Chondroid / Epithelial cells / Desmoplasia
o Secondary changes :
Calcification - Present / Absent
Metaplasia - Osseous / Chondroid
o Inflammatory cell reaction – Lymphocytes / Neutrophils / Histiocytes
/ Pigmented macrophages / Plasma cells / Giant cells
136
o Vascular invasion / Perineural invasion
S)Mitotic figures : Present - Typical / Atypical / Occasional / Frequent
• Absent
T) Necrosis: Present / Absent
U) Maturation of melanocytes: Present / Absent
V) Pagetoid spread to epidermis: present / Absent
W) Lymph node involvement: Present / Absent
X) Grading of tumour wherever applicable:
Benign
Malignant – Well / Moderately / Poorly differentiated
• Broders grading for SCC – Grade 1 / Grade 2 / Grade 3 / Grade 4
• Clark’s System of grading for Malignant Melanoma:
1 – Insitu / intraepidermal
2 – Papillary dermis
3 - Interphase
4 – Reticular dermis
5 – Subcutaneous fat
5) Histopathological diagnosis :
6) Special stains:
7) Final diagnosis:
137
KEY TO MASTER CHART
Sl.N - Serial No
Bx.N – Biopsy No
Ag – Age in years
Sx – Sex
• M – Male
• F – Female
Clinical Presentation
No : No of lesions
• S – Single
• M - Multiple
Site :
Pt S : Presenting Symptom
• U – Non healing ulcer
• S - Swelling
• N - Nodule
• P - Papule
• Up – Ulceroproloferative growth
• NU - Noduloulcerative
• F – Fungating mass
• W - Wart
• M - Mole
• P – Pigmented lesion
138
PH : Past history of similar lesion
• P- Present
• A – Absent
NS : Nature of specimen
• IB – Incisional biopsy
• EX – Excision
Gross Features
No : No of bits/specimen
• S- Single
• M – Multiple
Sz : Size of specimen or largest biopsy bit
Colour of lesion:
SK : Skin covering
• P-Present
• A- Absent
E/S: External Surface of specimen
• U- Ulcer
• Up- Ulceroproliferative growth
• V- Verrucous lesion
• P- Pigmented lesion
• G- Globular mass
• S- Smooth surface
C/S : Cut Section of lesion
• S- solid
• Cy- Cystic
139
• N – Nodular mass
• Pul – Pultaceous material
• H – Hair
Microscopic Findings
Location of lesion
• IE - Intra-epidermal
• Jn - Junctional
• ID - Intradermal
• Sc - Subcutaneous
• FT - Full thickness
TO : Origin of tumour
• E – Epidermal
• H - Hair Follicle Differentiation
• Se - Sebaceous Differentiation
• A - Apocrine Differentiation
• Ec - Eccrine Differentiation
• M – Melanocytic
Cir : Circumcription of tumour
• W - Well
• P - Poorly
• I - Infiltrative
• Pu - Pushing
Epidermis :
• U/R - Unremarkable
• H - Hyperkeratosis
140
• Pk - Parakeratosis
• Ac - Acanthosis
• Pa - Papillomatosis
• In - Invaginations
• ER- Elongated Rete Ridges
• BP - Bulbous Downward Proliferation
• DP – Downward Proloferation
• SP - Spinous Proliferation
• U - Ulcerated
• Th - Thinned out
• K - Koilocytic change
• A - Absent
• Pig - Pigment seen
KE: Keratinisation
• E - Epidermal Keratinisation
• T - Trichilemmal Keratinisation
• HC - Horn Cysts
• PHC - Pseudohorn Cysts
• KP - Keratin Pearls : M- Many / F- Few / O- Occasional
• Dy - Dyskeratotic cells
TE: Tumour connection with epidermis
• P – Present
• A – Absent
T Cells: Tumour Cells
• Sq - Squamous cells
141
• Ba - Basaloid cells
• N - Nevus cells
• M - Melanoma cells
• Se - Sebaceous cells
• Sh - Shadow
• Bp - Basophilic cells
• Gl - Glandular /Ductal epithelial cells
• C- Clear cells
C-Arr : Cell Arrangement
• IM - Irregular mass
• S - Sheets
• I - Islands
• N - Nests
• T - Tubular
• L- Lobules
• Co - Cords
• LL - lacelike
• Si - Singles
• Cy- Cystic
• Tr - Trabecular
• Pa - Papillary
• F - Fascicular
• Pp - Peripheral Palisading
• Cl - Clefting artifact
• SE - Squamous eddies
142
• Hy - Hyaline material
• Jp - Jigsaw puzzle
• Tp - Tadpole appearance
• Jn - Junctional activity
Cells:
• U - Uniform
• B - Biphasic
• T - Triphasic
• P - Pleomorphic
C-Sh : Cell Shape
• P - Polygonal
• R - Round
• O - Oval
• S - Spindle
• Co - Columnar
• Cu - Cuboidal
Nucleus:
• S - Small
• L - Large
• R - Round
• O – Oval
• Sp - spindle
• M - Monomorphic
• MP - Mildly pleomorphic
• P - Pleomorphic
143
Chr : Chromatin pattern
• N - Normochromatic
• H - Hyperchromatic
• F - Finely distributed
• C - Coarsely distributed
• V- Vescicular
Nuc : Nucleoli
• P – Prominent
• I – Inconspicuous
• Eo – Eosinophilic
• Ba – Basophilic
• A – Absent
Cyto : Cytoplasm
• S - Scanty
• M - Moderate
• A - Abundant
• Eo - Eosinophilic
• Ba - Basophilic
• C- Clear
• F - Foamy
• G - Granular
• Mp - Melanin pigment
• AS - Apical Snouts
CB : Cell Borders
144
• D – Distinct
• ID – Indistinct
S: Secretions
• P – Present
• A - Absent
Stroma:
• U/R - Unremarkable
• L- Loose
• D - Dense
• F - Fibroblastic
• M - Myxoid
• C - Chondroid
• Cal - Calcification
• Os - Ossification
• Ch - Cholestrol clefts
ICR : Inflammatory Cell reaction
• L - Lymphocytes
• N - Neutrophils
• H - Histiocytes
• PM - Pigmented macrophages
• P - Plasma cells
• G - Giant cells
MF : Mitotic Figures
• P- Present
• Ab – absent
145
• T - Typical
• A – Atypical
• F – Frequent
• O – Occasional
Nec: Necrosis
• P – Present
• A- Absent
MM : Maturation of melanocytes
• P – Present
• A – Absent
Pg E: Pagetoid spread to epidermis
• P - Present
• A – Absent
LN: Lymph node involvement
• P - Present
• A – Absent
HP Diagnosis: Histopathological Diagnosis
• SCC-Squamous cell carcinoma
• Ca-Carcinoma
• Ad BCC- Adnoid basal cell carcinoma
• Pg BCC-Pigmented BCC
• S BCC – Solid BCC
• Ker BCC – Keratotic BCC
• Inf BCC-Infiltrating BCC
• Baso-Sq Ca-Basosquamous carcinoma
146
• Verrucous Ca-Verrucous carcinoma
• Acanthotic SK-Acanthotic Seborrhoeic keratosis
• VV-Verruca vulgaris
• PTT- Proliferating trichilemmal tumor
• MPTT-Malignant proliferating trichilemmal tumor
• TE-Trichoepithelioma
• CS-Chondroid syringoma
• SCP-Syringocystadenoma papilliferum
• AH-Apocrine hidrocystoma
• IDN-Intradermal nevus
• MM-Malignant melanoma
Grading :
• B – benign
• M – Malignant
• Well – well differentiated
• Mod – moderately differentiated
• Poor – Poorly differentiated
Broders Grading Of SCC – Grade 1, Grade 2, Grade 3, Grade 4
Clark’s Grading of MM – Level 1, level 2, level 3, level 4, level 5.
SL.N Bx. N Ag Sx Clinical Presentation NS Gross features Microscopic FindingsNo Site Pt S PH No SZ Color SK E/S C/S Location TO Cir Epidermis KE TE T- cells Cell- Arr Cells C-Sh Nucleus Chr Nuc Cyto CB S Stroma ICR MF Nec MM PgE LN HP Diagnosis Grading BrodeClark
1 B2768/05 77 F S below eye S A IB S 1.2x1.4 GW A IE,SC E P U - A Ba S,I,T,D,Pp,Cl U O,S S"L,O,MP H A S,Ba,M ID A D,F,M L,H P,T,O A NA NA A Ad-BCC M2 B2792/05 70 F S lower eye lid P,N A IB M .4x.2x.1 GBr A ID E W U/R HC P Ba IM,I,Cy,Pp U O,S S,O,S H A S,Ba,M ID A D,F L,H P,T,O A NA NA A Pg,S-BCC M3 B3057/05 14 F S leg S A EX 3x2x1 GW A G S H W A T,Dy Sq IM,I,SE P P,R L,R.MP V P M,Eo ID A Cal P,T,O A NA A A PTT B4 B3270/05 20 F S upper eye lid P,N A EX M .2x.2x.2 GBr P ID M P Th A N S,N T 1 R S,R N A M,Eo,Mp D A U/R Ab A P A A IDN B
2 R,O S,R,O N A M,Eo,Mp ID3 O,S S,O,S N A M,Eo ID
5 B3413/05 55 M S foot Up A EX S 8x8x8 GW P Up S IE,ID E W,Pu H,Pk,Ac,BP E P Sq IM U P,R S,R N A A,Eo D A L L,H P,T,O A NA NA A Verrucous Ca M6 B3527/05 62 M S sole U P EX S 1.5x1 GBr P U S FT M W,I Th,H,pig,Jn P M S,I,N P R,O L,R,O,P C P,Eo M,Eo,Mp ID A U/R P,A,F A A A A MM M 47 B3530/05 40 M S scalp U A EX S 2.5x2x1 GW P U S ID H W U T,Dy Sq IM,I,Pp P P,R L,R,MP V I M,Eo ID A Cal Ab A NA NA A PTT B8 B4488/05 55 F S nose Up A IB M .5x.3x.2 GW A IE,ID E W,I Ac,H,ER KP-M P Sq I P P,R L,R,MP V P M,Eo D A U/R P,A,O A NA NA A SCC M- well 19 B4531/05 32 F S scalp S P Ex S 2x1x.8 GW-GBr A S S H W A T,Dy Sq IM,I,Pp P P,R, L,R,P V P M,Eo ID A U/R P,T,O A NA NA A PTT B
10 B4654/05 38 M S penis Up A IB M 1.5x1x.5 GW FT E P.I Ac,H,Pk,DP KP-M,Dy P Sq IM P P,R L,R,MP V P M,Eo D A D L,H P,A,O A NA NA A SCC M-well 111 B4671/05 79 F S lower eye lid N A EX M .5x.3x.2 GW ID E W Th,U Ba I,N,Cy,Pp,Cl U O,S S,O,Sp,M H A S,Ba,Mp ID A F L,H P,T,O A NA NA A Pg,S-BCC M12 B15/06 55 F S nose N A IB S 2x1x1 GW ID Se W U/R E A Se, Ba IM,L B 1 R S,R V P A,F D A D, Sq cells L,H,P P,T,O A NA NA A Sebaceoma B
2 R,O L,O H A S,Ba ID13 B475/06 14 F S face S A EX S 1x.5x.5 GW A S S H W A T Bp,Sh I B 1 R,O S,O H A S,Ba ID A D L,G Ab A NA NA A Pilomatricoma B
2 R shadow M,Eo ID14 B679/06 55 M S scalp N A EX S .8x.5x.4 GW P ID M P U/R A N S,N,Co B 1 R.O S,R N A M,Eo,Mp ID
2 O,S O,Sp N A M,Eo ID A PM Ab A P A A IDN B15 B821/06 35 F S angle of eye N A EX S 2x1.5x.8 GBr P ID,SC E P U Ba N,I,LL,T,Pp,Cl U O,S S,O H A S,Ba,Mp ID A D,M L,H P,T,O A NA NA A Ad-BCC M16 B952/06 58 M S foot sole Up A EX S 8x8 GW P Up S IE,ID E P,I Ac,H,Pk,DP KP-M,Dy P Sq IM P P,R L,R,MP V I M,Eo D A D L,H P,T,O A NA NA A SCC M-well 117 B1118/06 75 F S mouth angle U A EX M 2.5x2x1.5 GW-GY P IE E W,Pu Ac,H,PK,BDP E P Sq I U P S,R V I A,Eo D A D L,H Ab A NA NA A Verrucous Ca M18 B1206/06 35 M S scalp U A Ex S 4x4 GW P U S IE,ID E P,I U KP-M,Dy P Sq IM,S P P,R L,R,P V P M,Eo ID A D L,H P,A,F A NA NA A SCC M-Mod 319 B1287/06 28 F S scalp U P IB M 1x.5x.3 GW ID H P,I U T,Dy Sq IM,I P P,R L,R,P V P M,Eo ID A D,cal L,N,H,E P,A,F P NA NA A MPTT M20 B1383/06 59 M S forefoot U A IB S 3x1.5x1 GW P U S IE,ID E P,I Ac,H,DP KP-M,Dy P Sq IM P P,R L,R,P V P M,Eo D A D L,H P,A,O A NA NA A SCC M-well 121 B1393/06 40 M S penis Up A EX S 4x3 GW P U S IE,ID E P,I U KP-M,Dy A Sq IM,S P P,R L,R,P V P M,Eo D A D L,H P,A,F A NA NA A SCC M-mod 322 B1972/06 40 M S foot U A IB M 1x.8x.5 GW IE,ID E P,I Ac,H,DP KP-M,Dy P Sq IM P P,R L,R,MP V P A,Eo D A D L,H P,T,O A NA NA A SCC M-well 123 B2158/06 38 F S back P,N A EX S .8x.8x.4 GBr IE E E Ac,H,Pa HC,PHC P Sq,Ba B 1 P,R S,R N A M,Eo D A L L,H Ab A NA NA A AcanthoticSK B
2 O S,O H A S,Ba,Mp ID24 B2464/06 30 F S foot U A EX S 1x.8x.5 GW-GBr P ID M P U A N S,N B 1 R S,R N I M,Eo,Mp ID A Pm Ab A P A A IDN B
2 O,S S N I M,Eo,Mp ID25 B2547/06 40 M S leg U A Ex S 3x1.5x1 GW P U S ID E W U Ba N,I,T,Cy,Pp,Cl U O,S S,O H A S,Ba ID A F,M L,H,P P,T,O A NA NA A Ad-BCC M26 B2766/06 45 M S lower lid M A Ex S .3x.2x.1 GW ID M W U/R N S,N T 1 R S,R V I A,Eo,Mp D A PM Ab A P A A IDN B
2 R S,R N A M,Eo ID3 S S,Sp N A S,Eo ID
27 B2782/06 35 M S penis Up A IB S .4x.2x.1 GW IE,ID E I Ac,DP KP-M,Dy P Sq IM,I P P,R L,R,MP V P M,Eo D A D L,H P,A,O A NA NA A SCC M-well 128 B2869/06 22 F S upper lip M A EX S .3x.2x.1 GBl P ID M P U/R A N S,N,Co T 1 R S,R V I A,Eo,Mp D A PM Ab A P A A IDN B
2 R S,R N A M,Eo ID3 S S,Sp N A S, Eo ID
29 B3475/06 60 M S ear P,N A EX S .5x.3x.2 GBr P IE E W Ac,Pa,ER E P Sq,Ba B 1 P S,R N I M,Eo ID A D L,PM Ab A NA NA A Acathotic SK B2 O L,O H A S,Ba,Mp ID
30 B3607/06 60 M S flank W A EX S .8x.5x.4 GBr P V S IE E W Ac,H,Pa HC,PHC P Sq,Ba B 1 P S,R N A M,Eo ID A Ab A NA NA A Acanthotic SK B2 L,O H A S,Ba,Mp ID U/R
31 B3611/06 40 M S groin P,N A EX S 2x2 GBr P V S IE E W Ac,,DP E,HC,PHC P Sq,Ba B 1 P S,R N I M,Eo ID A D L,PM Ab A NA NA A Acanthotic SK B2 O L,O H A S,Ba,Mp ID
32 B3772/06 65 M S penis U A IB M .8x.4x.2 GW ID E I U,Ac,DP KP-F,Dy P Sq IM P P,R L,R,P H I M,Eo ID A D L,H,N P,A,F A NA NA A SCC M-mod 233 B3917/06 62 M S penis S A EX S 5x2 GW P U S ID E I U KP-O,Dy P Sq IM P P,R L,P H,V P M,Eo ID A D L,N,H P,A,F A NA NA A SCC M-mod 334 B155/07 28 F S ear lobe Up A EX S 1x.5 GW-GBr P Up S,N FT M W U,Th M S,N,F,Jn P R,O,S L, V P,Eo M,Eo,Mp ID A D L,PM P,A,F A A P A MM M 435 B684/07 37 M S cheek Up A IB M .3x.2x.1 GW ID E I A KP-F,Dy Sq IM,I,Si P P,R L,P V P M,Eo D A D L,H,N P,A,O A NA NA A SCC M-well 236 B1222/07 50 F S lower lip F A IB S .5x.4x.3 GW P ID E I H,Pk,In,DP KP-M,Dy P Sq IM P P,R L,R,MP V P M,Eo D A L,N,H P,A,O A NA NA A SCC M-well 137 B1566/07 60 M S foot S A EX M 2x1.5x1 Bl,GW S IE,ID,Jn M P Ac,Th,U P M S,N,Jn P R,O,S L,P V P,Eo M,Eo,Mp ID A D L,N,PM P,A,F A A A A MM M 438 B1787/07 25 F S nip & areola U A IB S 1x.5x.2 GW P IE,ID E I Ac,DP KP-F,Dy P Sq IM,I P P,R L,R,MP V P M,Eo D A L,H,N P,A,O A NA NA A SCC M-well 239 B2027/07 60 M S penis Up A IB M 1x.5x.3 GW IE,ID E P,I Ac,H,Pk KP-M,Dy P Sq IM P P,R L,R,MP V P M,Eo ID A D L,H,P P,A,O A NA NA A SCC M-well 140 B2099/07 75 F S cheek Up A EX S 1x1x1 GW P Up Ec W A Gl L,T,Cy B 1 P,R S,R,O N I A,C D P P,T,O A NA NA A Hidradenoma B
2 O O H A S,Eo ID41 B2238/07 43 F S vulva V A EX M 1x.5x.5 GBr-GBl V IE E W Ac,Pk,H,ER,K Sq U P S,R N I A,Eo D A D L,H Ab A NA NA A VV B42 B2315/07 60 M S penis U A IB S 1x.8x.8 GW IE,ID E P,I Ac,H,Pk,U,DP KP-F,Dy P Sq IM P P,R L,R,MP V P M,Eo D A L L,H P,A,O A NA NA A SCC M-well 143 B2318/07 25 F S face M A Ex S .5x.4x.3 GBr ID M P U/R A N S,N,Co,Cl T 1 R S,R V I A,Eo,Mp D A U/R A A P A A IDN B
2 R S,O N A S,Eo ID3 S S,Sp N A S,Eo ID
44 B2600/07 70 M S foot Up A EX S 4x4x4 GBr P U S FT M P,I U P M S,N,Jn P R,O,S L,P V P,Eo M,Eo ID A L,H,PM P,A,O A A P A MM M 445 B2994/07 60 M S foot Up A EX S 18x13 GW P Up S IE,ID E P,I Ac,U,DP KP-M,Dy P Sq IM P P,R L,R,MP V P M,Eo ID A D L,N,M,P P,A,F A NA NA A SCC M-well 146 B3052/07 65 M S calf W A EX S 1.5x.5x.5 GBr IE E W Ac,Pk,H,K P Sq U P,R S,R N A A,Eo D A L,H A A NA NA A VV B47 B3189/07 70 F S nose NU A IB M .3x.2x.1 GW-GBr ID E W Ac HC Ba N,I,PP,CA U O L,O,M H A S,Ba ID A D L,PM P,T,O A NA NA A Pig,S-BCC M48 B3306/07 55 M S back S A EX S 2x1x.5 GW P S S,Cy ID Ec W U/R A S,I,T,Cy B 1 R S,R N A M,C ID P Ab A NA NA A Hidradenoma B
2 R S,R N I M,Eo ID49 B3449/07 55 M S cheek NU A IB M .3x.2x.1 GBr ID E W U/R Ba N,I,Pp,Cl U O S,O,M H A S,Ba ID A F L,H P,T,O A NA NA A Pig,S-BCC M
50 B3477/07 47 M S penis Up A EX S 3x2x1.5 GW P Up S FT E P,I Ac,DP Dy P Sq IM P R,P L,R,P V P M,Eo ID A D L,H,P,G P,A,F P NA NA A SCC M-mod 351 B3481/07 55 M S penis N A IB M 1.5x1x.5 GW P FT E P,I Ac,H,DP KP-M,Dy P Sq I P P L,R,MP V P M,Eo D A D L,E,H,P P,A,O A NA NA A SCC M-well 152 B3622/07 55 M S lower lid NU A EX M 3x2x.5 GW-GBr ID E W U T,HC P Ba N,I,Pp,Cl U O S,O H A S,Ba,Mp ID A M, Sq cells L,N,H P,T,F A NA NA A Ker-BCC M53 B3983/07 27 M S lower lip U A EX S 1.5x1x.5 GW P U S FT E P,I U,Ac,Pk,DP KP-M,Dy P Sq IM,S P P L,R,MP V P M,Eo D A L L,H P,A,O A NA NA A SCC M-well 154 B30/08 42 M S sole S A EX S 4x4x3 GW P N S IE E W,Pu Ac,Pk,H,In,Bp E P Sq U P S,R,M V P A,Eo D A L,H P,T A NA NA A Verrucous Ca M55 B106/08 32 F S scalp S A EX S 2x1.6x1.5 GW P N N ID Ec W U/R A Gl I,T,Pp,Jp,Hy B 1 R,O L,R,O V A M,Eo ID P L A A NA NA A Cylindroma B
2 O S,O H A S,Eo ID56 B237/08 62 M S penis Up A IB S 1.3x.7x.2 GW FT E P,I Ac,Pk,H,DP KP-M,Dy P Sq IM P P,R L,R V P M,Eo D A D L,H P,A,O A NA NA A SCC M-well 157 B408/08 40 F S forehead U A IB M .3x.2x.2 ID E I Ac,Pk U P Ba N,Tr,Pp,Cl U O,S S,O,M H A S,Ba,Mp ID A L,F,M L,PM P,O A NA NA A Pig,S-BCC M58 B1007/08 78 M S lower lid S A IB S 1x.6x.2 GW-GBr P ID,Sc Se P,I Th A Se,Ba L,N,Pp B 1 P,R L,R,P V P M,F,C ID A L,H P,A,O A NA NA A Sebaceous Ca M- mod
2 O L,O H A S,Eo,C ID59 B1305/08 72 F S chest wall P,N A EX S 2x1x.5 GBl P N S IE E W Ac,H,Pk,Pa,ER P Ba U O S,O,M H A S,Ba,Mp ID PM,L Ab A NA NA A Acanthotic SK B60 B1538/08 10 M S forefoot V A EX S .8x.5 GW IE E W Ac,H,Pk,Pa E Sq U P S,R,M N A A,Eo D A Ab A NA NA A VV B61 B1540/08 45 M S popliteal U A IB M 2x1x1 GW E P,I U Dy Sq S,F P O,S L,O,Sp,P V P M,Eo ID A U/R P,A,F P NA NA A SCC M-poor 462 B1720/08 45 F S axilla U A IB M .5x.5x.4 GW ID Ec P U A Gl N,Co,Cy B R,P S,R,MP V P M,A,Eo,C ID A D L,N P,O A NA NA A Hidradenoma B63 B1721/08 40 F S occipital U A IB M 1x.8x.2 GW ID H P U,Ac T A Sq I P P L,R,MP V P M,Eo ID A U/R P,T,O A NA NA A PTT B64 B1754/08 65 M S foot V A EX S 1x1x1 GBr P IE E W,Pu Ac,H,Pk,BP E P Sq U P S,R,M V I M,Eo D A L,H Ab A NA NA A Verrucous Ca M65 B1938/08 42 F S pinna S A EX S 1x1x1 GW P ID M P U/R A N N,T,Co,L T 1 R S,R,M N I A,Eo,Mp D A U/R Ab A P A A IDN B
2 R S,R N A M,Eo ID3 S Sp N A M,Eo ID
66 B2047/08 50 M S penis Up A EX S 6x5x3 GW P Up S FT E p,I Ac,Pk,DP,U KP-M,Dy P Sq IM,I,Co P P,R L,R,P H I S,Eo ID A U/R P,A,F P NA NA A SCC M-mod 367 B2093/08 70 M S ear front U A EX S .3x.2x.1 GBl P U S FT E P,I U Ba I,N,Pp,Cl U O,S S,O,MP H A S,Eo ID A D,M PM P,T,O A NA NA A Pig, S-BCC M68 B2377/08 75 M S penis U A EX M 1x.5x.3 GW FT E P,I Ac,H,Pk,DP HC,KP-M,D P Sq IM,I P P,R L,R,MP V P M,Eo ID A D L,H P,A,O A NA NA A SCC M-well 169 B2518/08 60 M S lower lip Up A IB M .5x.4x.1 GW FT E P,I Ac,H,Pk,ER KP-M,Dy P Sq IM P P,R L,R,MP V P M,Eo D A U/R P,A,O A NA NA A SCC M-well 170 B2602/08 18 F S abd wall S A EX S 2x1x.5 GW-GY ID,Sc Ec W A G L,Cy,Hy B 1 R S,R,M H A A,C D P U/R Ab A NA NA A Hidradenoma B
2 R,P S,R,M N A M,Eo ID71 B2611/08 60 M S axilla S A EX S 2x1.5 GW P N S ID H W Th T A Sq IM,I P P,R L,R,MP C I M,Eo ID A Cal L,H,G P,T,O A NA NA A PTT B72 B2664/08 80 F S nose N A EX M .6x.5x.2 GW ID H W Th HC A Ba N,LL,Pp U O,S L,O H A S,Ba,Mp ID A F PM Ab A NA NA A TE B73 B2666/08 62 M S face U A EX S 1.5x.5 GW P U S ID E P,I Th HC Ba N,I,Pp,Cl U O,S S,O,MP H A S,Ba ID A F L,H P,A,O A NA NA A Ker-BCC M74 B2758/08 60 M S lower lip U A IB M .8x.5x.3 GW FT E P,I Ac,Pk,H,DP KP-F,Dy P Sq IM P P L,R,MP V P M,Eo D A D L,H P,A,O A NA NA A SCC M-mod 275 B2872/08 45 M S scalp U A IB M 1.2x.6x.3 GW ID E P,I Ac,In,DP KP-M,Dy,HCP Ba, Sq IM,N,I B 1 O O,Sp H A S,Ba ID A D,F L,N,PM P,A,O P NA NA A Baso-Sq Ca M
2 P,R L,R,MP V P M,Eo ID76 B3060/08 50 M S forehead U A EX M 3.5x2x.3 GW P U S ID E P,I U Ba I,Pp,Cl U R,O S,O,MP H A S,Ba ID A F,M L,H P,T A NA NA S-BCC M77 B3093/08 52 M S heel U A EX S 5x3.5 Bl P U S FT M P,I Ac,Th,Pk,H,U P M S,N,Jn P R,S L,O,P V P,Eo M,Eo,Mp ID A L,H,PM P,A,F A A A A MM M 478 B3221/08 27 M S lip Up A EX S 4.5x3.5x2 GW P Up S IE E W Ac,Pk,H,BP E P Sq U P S,R V P M,Eo D A L,H A A NA NA A Verrucous Ca M79 B3575/08 48 M S forehead S A EX S 1x1x1 GW P ID Ec W U/R A Gl I,Co,T B 1 R S,R,M H A S,Eo ID P L,M L, A A NA NA A CS B
2 R,P S,R,M N A M,C ID80 B3665/08 61 M S foot W A EX S 2.5x1.5x.5 GW P W S IE E W Ac,H,Pk,ER E Sq U P,R S,R,N N A A,Eo D A Ab A NA NA A VV B81 B3803/08 38 M S back S A EX S 3x2x1 GW-GY P N ID A W Ac,Pa,In P Gl Pa,Cy B 1 Co S,O N I A,Eo,AS D P U/R P,L Ab A NA NA A SCP B
2 Cu S,R N A S,Eo D82 B3844/08 15 F S foot W A EX S 2.5x2x1 GBl P W S IE E W Ac,H,Pk,K P Sq U P S,R,M V I A,Eo D A L,H Ab A NA NA A VV B83 B4064/08 60 F S foot Up A EX S 5x5x3 GW P Up S IE,ID E P,I Ac,H,DP,U KP-M,Dy P Sq I P P,R L,R,MP V P M,Eo D A D L,G P,A,O A NA NA A SCC M-well 184 B4090/08 55 M S back S A EX S 5x3x2.5 GW-GBr N S ID E I U/R A Ba L,LL,Pp,Cl,SE U O,S L,O,MP H A S,Ba ID A F L,PM P,A,O A NA NA A BCC M85 B211/09 55 F S penis Up A EX S 1x1x1 GW P Up S IE E W Ac,H,Pk,BP E P Sq U P S,R N A A,Eo D A D L P,T A NA NA A Verrucous Ca M86 B430/09 58 F S foot U A IB M 1.5x.5x.3 GW IE,ID E P,I Ac,DP,U KP-M,Dy P Sq IM,I P P,R L,R,MP V P M,Eo D A U/R L,H,E P,A,O A NA NA A SCC M-wel 187 B539/09 49 M S foot U A EX S 3x2x1 GW-GBr P IE,ID E P Ac,Pa,ER Dy P Sq U P,R L,R,MP V P M,Eo D A U/R L P,T A NA NA A PEH B88 B696/09 60 M S sole S A EX S 7x4x1 Bl P S ID M P,I H, ER,Mp P M N,S,Jn P R R,P V P,Eo M,Eo,Mp ID A U/R PM P,A,O A A P P MM M 389 B759/09 30 F S foot U A IB M .6x.4x.3 GW IE,ID E P,I U KP-M,Dy P Sq IM,I P P,R L,R,MP V P m,Eo ID A Cal P,A,O A NA NA A SCC M-well 190 B904/09 65 F S cheek N A IB S .3x.3x.2 GW ID E P,I U P Ba N,Pp,Cl U R,O,S S,O H A S,Ba ID A F,M PM P,A,O A NA Na A S-BCC M91 B1199/09 65 F S lower lip U A IB M .5x.3x.2 GW P E P,I Ac,U,DP OKP P Sq IM,I,Si P P,R L,R,P C P M,Eo ID A D L,PM P,A,F A NA NA A SCC m-mod 292 B1427/09 62 M S leg U A IB M .6x.6x.4 GW E P,I A KP-M,Dy Sq IM,I P P,R L,R,MP V P M,Eo D A U/R P,A,O A NA NA A SCC M-well 193 B1467/09 45 M S neck U A IB M 1.5x1x.5 GW FT E P,I U KP-M,Dy P Sq IM,I P P,R L,R,MP V P M,Eo D A P,A,O A NA NA A SCC M-well 194 B1655/09 45 F S vulva Up A EX S 3x3x1 GW P Up S IE,ID E P,I Ac,Pk,H,DP KP-M,Dy P Sq I P P,R L,R,O V P M,Eo D A U/R P,O A NA NA A SCC M-well 195 B1666/09 60 M S axilla Up A EX S 6.5x6x3.5 GW P Up S ID,Sc A P,I U Gl IM,S,I,T,Si P R L,R,P V P A,Eo,C,G ID A U/R P,A,F P NA NA A Apocrine Ca M96 B1707/09 55 M S foot Up A IB M 1.5x1x.5 GW IE,ID E I Ac,H,DP KP-M,Dy P Sq IM P R,O L,R,MP V P M,Eo D A L,H P,O A NA NA A SCC M-well 197 B1826/09 55 M S penis U A EX S 3x2x1 GW A U S E P,I Ac,H,Pk,DP KP-M,Dy Sq IM,I P R,O L,R,O V P M,Eo D A D N,H P,A,O A NA NA A SCC M-well 198 B1884/09 27 F S scalp S A EX S 2x2x1 GW-GY A N S ID H W U/R T A Sq I,Pp P P,R R V P M,Eo ID A F P,T,O A NA NA A PTT B99 B1979/09 55 M S penis U A IB M 1x.4x.3 GW ID E P,I U KP-F P Sq IM,I,Co P P,R L,R,MP V P M,Eo ID A P,O A NA NA A SCC M-mod 3
100 B1995/09 73 M S perianal Up A IB M 2x.5x.5 GW-GBr E P,I A KP-F Sq IM,I P P,R L,P H A M,Eo ID A Cal P,A,F P NA NA A SCC M-mod 2101 B2177/09 50 F S eye lid S A EX S 1.5x1x.5 GW P N S ID E P,I U/R P Ba N,Cy,Pp,Cl U O,S S,O,Sp H A S,Ba ID A P,T,O A NA NA A S-BCC M102 B2275/09 50 M S foot Up A EX S 4x2.5x2 GW P Up S IE,ID E W Ac,H,Pk,DP KP-M P Sq I P P L,R,MP V P A,Eo D A D L,N P,A,O A NA NA A SCC M-well 1103 B2332/09 57 M S back S A EX S 1.2x1.2x1 GW P ID Ec W U/R A Gl S,T,Co U R S,M N A M,Eo ID P Ab A NA NA A Hidradenoma B104 B2468/09 30 F S leg U A IB S .8X.4X.2 GW E P U KP-F,Dy Sq IM,Si P P,R L,P V P M,Eo D A L L,M P,A,O A NA NA A SCC M-mod 2105 B2591/09 27 F S eyelid N A EX S .3X.2X.1 GW ID Ec W U/R Gl N,T,Tp U R,O S,R,O,M N A S,Eo ID P L,F Ab A NA NA A Syringoma B106 B2949/09 30 M S lower lip U A IB M .8x.5x.3 GW FT E P,I Ac,DP KP-M,Dy P Sq IM,I P P,R L,R,MP V P M,Eo D A Cal L,H P,O A NA NA A SCC M-well 1107 B3000/09 65 M S chest U A EX S 4.5x3x1.8 GW-Bl P U S ID E P U P Ba N,Pp,Cl U O,S S,O,Sp H A S,Ba,Mp ID A D,M,F L,N,PM P,O A NA NA A Pig-BCC M108 B3484/09 65 M S post auricular U A IB S 1x.4x.4 GW P ID E P U P Ba N,I,Pp,Cl U O,S S,O,Sp H A S,Ba ID A F L,PM P,O A NA NA A Pig-BCC M109 B3491/09 60 F S forehead U A EX S 4x3 GW P U S ID Ec W U/R A Gl I,N,Cy B 1 P,R S,R N A A,C ID A D, Sq diff L,N Ab A NA NA A Hidradenoma+Sq B
2 R S,R N A M,Eo ID differentiation
110 B3771/09 35 F S axilla S P EX S 7x7x7 GW P G Cal,SID H W U/R T A Bp,Sh IM B 1 R,O S,O H A S,Ba ID A Cal L Ab A NA NA A Pilomatricoma B2 R,P shadow M,Eo ID
111 B3864/09 35 M S thigh V A EX S 1.5x1.5x1 GW P V S IE E W Ac,Pa,H E P Sq U P S,R V I A,Eo D A D L Ab A NA NA A VV B112 B3865/09 45 M S abdomen wall U A EX S 5x5x3 GW P N S ID Ec W Ac, clear cell change P Gl L,S U R L,R,MP V I M,C,Eo ID A P,A,O A NA NA A Hidradeno Ca M113 B4015/09 35 M S face M A EX S 1x.7x.7 GBl P S S ID M P U/R A N S,N,Co B 1 R S,R N A M,Eo ID A U/R Ab A P A A IDN B
2 O,S S,O,Sp N A M,Eo ID114 B4276/09 50 M S heel U A EX S 5x5x5 GW P U S IE,ID E I Ac,H,Pa,ER KP-M P Sq IM,I P P,R L,R,MP V P A,Eo D A D L,H P,A,O A NA NA A SCC M-well 1115 B187/10 40 M S penis Up A IB S 6x2.5x1 GW S FT E P,I Ac,Pk,H,DP KP-M,Dy P Sq IM,S P P,R L,R,P C P M,Eo D A D L,N,P,H P,A,O A NA NA A SCC M-mod 1116 B98/10 38 M S leg S A EX S 1x1x1 GW P N S ID H W U/R T A Bp,Sh IM,I,Pp B 1 O,S S,O N A S,Ba ID A L,Cal L,N,H,G Ab A NA NA A Pilomatricoma B
2 R,P shadow M,Eo ID117 B204/10 48 M S penis Up A EX S 3x2x1 GW P Up S FT E I U,Ac,H,DP KP-M,Dy P Sq IM,I P P,R L,R,MP V P M,Eo D A L,H P,A,O A NA NA A SCC M-well 1118 B302/10 40 M S foot sole Up A EX S 6x6x2 GW P Up S IE E W Ac,H,Pk,Pa,BP E P Sq U P S,R,M N A A,Eo D A L,H Ab A NA NA A Verrucous Ca M119 B401/10 30 F S eyebrow S A EX S 1x1x1 ID M P U/R A N S,N,Co T 1 R S,R F I A,Eo,Mp D A U/R Ab A P A A IDN B
2 R,O S,O N A M,Eo,Mp ID3 O,S S,O,Sp N A S,Eo ID
120 B973/10 65 M S mouth angle Up A EX S 3x2x1 GW IE E W Ac,H,Pk,BP E P Sq U P L,R,MP V P A,Eo D A D L,H P,T,O A NA NA A Verrucous Ca M121 B1058/10 11 F S scalp S P EX S 6x5x3 GW P N S W U/R A Gl L,S,T U R L,R,MP V I ID P U/R P,A,O A NA NA A Hidradeno Ca M122 B1084/10 75 F S eye brow S P EX S 2x2x2 GBr P N S,Cy ID,Sc E W U KP-M A Sq S,I,Cy P P,R L,R,P V P M,A,Eo D A L,H,G P,A,O A NA NA A SCC M-mod 2123 B1111/10 62 M S auditary canal Up A EX S 2.5x1x.5 GW S FT E,A P,I U,Ac,DP KP-M,Dy P Sq,Gl IM,Cy B 1 P P,R,P V P M,Eo ID P L,H P,A,O A NA NA A SCC+ AH M-well 2
2 Co S,R,M N A A,Eo,AS D A124 B1142/10 67 M S penis Up A EX M 1x1x.5 GBr FT E P,I Ac,H,Pk,DP KP-M P Sq IM,I P P,R L,R,MP V P M,Eo D A L,H P,A,O A NA NA A SCC M-well 1125 B1229/10 65 M S foot U A IB M 1x.4x.3 GW FT E P,I Ac,H,DP KP-M,Dy P Sq IM,I P P,R L,R,MP V P M,Eo D A P,A,O A NA NA A SCC M-well 1126 B1263/10 26 F S face S A EX S 2x1x.3 GBr N S H W T Bp,Sh IM,I B 1 R,O S,O N A S,Ba ID A U/R Ab A NA NA A Pilomatricoma B
2 P,R shadow A,Eo D127 B1304/10 67 M S penis Up A EX S 3X3X3 GW P Up S IE,ID E I Ac,Pa,DP KP-M,Dy P Sq I P P,R L,R,MP V P M,Eo D A P,A,O A NA NA A SCC M-well 1128 B1431/10 58 M S inguinal Up A IB S 1X1X.8 GW ID E P,I U KP-F,Dy P Sq IM,I P P,R L,R,P C P M,Eo D A L,H P,A,F A NA NA A SCC M-mod 2129 B1433/10 82 M S cheek NU A EX S 3x.7 GW P U S ID E W U P Ba N,I,LL,Pp,Cl U R,O S,O,M H A S,Ba ID A L,M L,N,H P,T,F A NA NA A Ad-BCC M130 B1574/10 75 F S forehead NU A IB M 1.2x.5x.2 GW ID E P U P Ba I,Co,Pp,Cl U R,O S,O,MP H A S,Ba ID A L,F,M,D L,N,H P,A,T A NA NA A Inf-BCC M131 B1727/10 12 F S ear M A EX M .3x.3x.2 GBr ID,Jn M P Th,Jn P N N,S,Co T 1 R S,R N A M,C,Mp ID A Ab A P A A Compound Nevus B
2 R,O S,R N A M,Eo,Mp ID3 O,S Sp N A M,Eo,Mp ID
132 B1983/10 50 F S face S A EX S .8x.5x.3 GW ID H W U/R HC A Ba I,PP U O S,O H A S,Ba ID A F Ab A NA NA A TE B133 B1894/10 65 M S foot U A EX S 5x4x3 GW P U S IE,ID E P Ac,H,DP KP-M,Dy P Sq IM P P,R L,R,P V P M,Eo D A U/R P,A,O A NA NA A SCC M-well 1134 B2072/10 60 F S eye lid S A EX S .6x.5x.4 GW Se P,I A Se S,L P R L,R C P A,F D A P,A,F P NA NA A Sebaceous Ca M- well
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