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PROPERTI SEL TUMOR
Dr. HUMAIRAH MEDINA LIZA LUBIS, M. Ked .(PA), Sp.PA
DEPARTEMEN PATOLOGI ANATOMI
FAKULTAS KEDOKTERAN
UNIVERSITAS BATAM
BATAM - 2012
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Normal Cells
Attach to each other by various cell junctions so that they are
fixed in place
Communicate with each other via Growth Factors
Stimulatory growth factors turn on genes called
protooncogenes
Inhibitory growth factors turn on Tumor Suppressor Genes
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3/12/2014
Cellular Growth Control
Balance proliferationcell differentiationcell death
Proliferation determined through cell cycle
Cellular growth control by genetic : proto-oncogen
supressor gen
apoptosis and
DNA repair in cell cycle
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3/12/2014
Abnormal Growth
Atrophy: size of the cells decreased
Diffuse atrophyimmobilitation
Denervation atrophy : poliomyelitis
Loss of Trophic hormon : Breast, endometrium atrophy
Lack of nutrition : Kwashiorkhor
Senile atrophy : Brain atrophy
Hypertrophy: size of the cells increased
Physiologic hypertrophy
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Hyperplasia: Means too much cell proliferation or mitosis.
This is abnormal but not cancer
Dysplasia: A cell is not only proliferating excessively, but
attains abnormal and orientation; Pre-cancerous
Neoplasia: New aggressive growth of cells and tissues
putting pressure on neighboring tissues (Causing
abnormal swelling or tumor) or invading neighboring
tissues (cancer)
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More TERMS:
Metaplasia: conversion of one cell type into another, such as, stratified
oesophagus or lung tissues (due to acidity or cigarette).The process is reversible
and is not cancer, but may lead to cancer.
Metastasis: Spreading to distant sites.
- First site where cancer is detected is called primary site and the second
site, secondary site.
- Small clumps of cancer cells (emboli) Spread by migration throughblood (called blood-borne or hematogenous) or through lymphatics
(lymphogenous).
- Cancer cells spread because they lose their molecular address where to
go
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Anaplasia: Primitive undifferentiated state of cell growth
Aplasia: A loss of normal appearance and
disorganizations of tissues
In situ cancer: abnormal growth at a particular site but no
invasion of neighboring tissues
Invasive cancer: Lethal and malignant as neighboring
tissues are invaded
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Karakteristik NeoplasmaJinak Ganas
Neoplasma dapat dibedakan menjadi jinak / ganas,berdasarkan:
Differensiasi & anaplasia Kecepatan pertumbuhan (rate of growth)
Invasi lokal (local invasion)
Metastasis (anak sebar)
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1. Differensiasi & anaplasia
Differensiasi:derajat kemiripan sel neoplastik (selparenkim tumor) dengan sel normal. Makin mirip makin baik differensiasinya.
Well differentiated Moderately differentiated Poorly differentiated undifferentiated
Semua tumor jinak --- tersusun dari sel neoplastikyang mirip dengan sel normal (well differentiated) Tumor ganas bisa: well differentiated s.d
undifferentiated.
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Anaplasia--- menunjukkan pertumbuhan ke arahtingkatan lebih rendah atau hilangnya differensiasi
struktural & fungsional suatu sel normal Anaplasia --- hallmark of malignant transformation
(petanda tumor ganas)
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Ciri-ciri morfologik sel anaplastik Pleomorfik: ukuran & bentuk bervariasi (variation in
size & shape). Sel bisa berukuran >> besar atau >) Rasio inti : sitoplasma (N/C ratio) (hampir 1:1)
(normalnya N/C ratio 1:4 atau 1:6) Butiran kromatin kasar Nukleoli (anak inti) nyata/ prominent
Mitosis: jumlah > & didapatkan mitosis atipik. Hilangnya polaritas: gangguan orientasi susunan
sel dalam jaringan.
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Sel anaplastik
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DYSPLASIA
Artinya: disordered growth Terutama pada sel epitelial, ditandai oleh hilangnya
uniformitas individual sel & hilangnya orientasiarsitektur normal sel dalam jaringan
Morfologi: Pleomorfisme (+)
Inti hiperkromatik (+)
Mitosis meningkat
Derajat dysplasia Displasia ringan (mild dysplasia)
Displasia sedang (moderate dysplasia)
Displasia berat (severe dysplasia) = Carsinoma insitu.
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Dysplasia cervix
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2. Kecepatan pertumbuhan
(rate of growth) Secara umum:
Kebanyakan tumor jinak: tumbuh lambat
tergantung hormon & supply darah
contoh: leiomyoma uterus akan tumbuh cepat jikaestrogen >> (kehamilan)
Kebanyakan tumor ganas: tumbuh cepat.
Secara umum, kecepatan pertumbuhan tumorberhubungan dengan derajat differensiasinya
kebanyakan tumor ganas tumbuh lebih cepat
daripada tumor jinak
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3.Invasi lokal (local invasion)
Tumor jinak
Tumbuh lokal& tidak mempunyai kemampuan untukmenginfiltrasi, menginvasi jaringan sekitarnya.
Berbatas jelasdengan jaringan sekitar, mempunyaikapsul(simpai) ataupun pseudocapsul(simpai semu).
Tidak metastasis(tidak beranak sebar)
Pengecualian: hemangioma (tumor jinak pembuluh
darah)tidak berkapsul & tumbuh seperti
infiltratif dalam jaringan.
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Leiomyoma uteri
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Tumor ganas:
Tumbuh progresif, invasi & infiltrasike jaringansekitarnya.
Batas tidak jelas & tidak berkapsul
Pengecualian: tumor ganas yang tumbuhnya lambat
bisa terlihat berbatas jelas pada makroskopis,namun secara mikroskopis akan terlihatpertumbuhan yang infiltratif ke jaringan sekitar.
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Beberapa kanker dapat tumbuh dari suatu lesipreinvasif, disebut sebagai Carcinoma insitu.
Biasanya terjadi pada cervix, kulit, mamma.
Ca insitu menunjukkan gambaran sel ganas tetapitidak menginvasi membran basal (basal membraneintak).
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4. Metastasis
Adalah anak sebar ke jaringan yang jauh dari tumorasal.
Merupakan petanda keganasan yang paling kuatdiantara tanda lain:
Tumorjinak --- tidak metastasis
Tumor ganas --- metastasis
Metastasis:
Percontinuatum
lewat rongga Limfogen
Hematogen
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Metastasis per continuatum: Lewat rongga tubuh (body cavity)
Contoh: Ca ovarium --- ke peritoneum
Ca colon --- ke cavum peritoneum
Ca paru --- ke cavum pleura
Metastasis secara limfogen:
Terutama pada carcinoma
Pola penyebaran metastasis kelenjar limfemengikuti rute normal dari lymphatic drainage.
contoh: Ca mamma - metastasis KGB axilla
Ca paru metastasis ke KGB hilus
Ca nasofaringmetastasis KGB colli
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Metastases secara hematogen
Terutama pada sarcoma
Dapat juga terjadi pada carcinoma Renal cell ca --- vena renalis
Penetrasi ke vena > arteri, karena arteri memilikidinding > tebal lebih tahan
Invasi pada vena --- sel tumor mengikuti aliran vena --- metastasis sering terjadi pada paru & hepar
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Hepar yang mengandung metastasis kanker
P b di t t ji k &
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Perbandingan antara tumor jinak & ganas(contoh: leiomyoma >< leiomyosarcoma)
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Classification:
Carcinoma: cancer of epithelial tissues
Adenocarcinoma: cancer of glandular tissue; spread through lymphatics
Sarcoma: cancer of stromal or mesenchymal layers of organs; spread via blood
Carcinosarcoma: mixtures of cancer cells from both epithelia and mesenchma
Teratoma: cancer of stem cells
Undifferentiated neoplasms: poorly undifferentiated
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Characteristics of cancer cells
1. Infiltration and destruction of surrounding tissues
2. Loss of contact inhibition of growth
3. Variation in shapes and sizes based on degree of differentiation4. Uncontrolled mitosis or cell proliferation or growth rate. Less
dependent on growth factors
5. Often migration to distant sites and loss of similarity with parent
tissues
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Cancer classification
Sporadic cancer:
Cancer without a family
history; non-hereditary andnot affecting off-springs
- Mutations not present inthe germline cells.
- Colon cancer mostlysporadic
Hereditary cancer:
Mutations are present in
the germline cells and
predispose to
inheritance towards
developing cancer
(familial).
Breast cancer is an
example
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Properties of Cancer Cells
Unlimited Replicative Potential
Absence of Apoptosis
Absence of Telomere Shortening
Angiogenesis
Metastasis
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Unlimited Replicative Potential
Cancer Cells Escape Regulation of the Cell Cycle
proto-oncogenes become oncogenes
ex: ras family of genes (mutated in lung, colon, andpancreatic cancers)
tumor suppression genes inactivated, or cell fails torespond
ex: RB tumor suppressor gene fails to function (breast,prostate, bladder, and other cancers)
ex: mutated p21 gene product no longer binds to cyclin,thus cyclin-dependent kinase uninhibited and celldivision uncontrolled
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Cancer cells differently from
normal cells
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Absence of Apoptosis
most often caused by damage to p53 gene that triggers
apoptosis
cells do not respond to normal triggers of apoptosis such
as metabolic stress or oxygen deprivation
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Absence of Telomere Shortening
telomerase allows cells to rebuild telomeres (prevents them
from being used up
gene for telomerase turned on in cancer cells
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Angiogenesis
formation of new blood vessels
vascular endothelial growth factor (VEGF) stimulatesblood vessel growth
Cancer cells release VEGF
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Metastasis
Cancer cells produce proteinase enzymes that allow them to
invade blood and lymphatic vessels and move about the body
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Metastatic Cancer
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Causes of Cancer
Heredity
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Heredity
mutated tumor suppressor genes can beinherited
ex: BRCA1 (breast cancer gene # 1)
ex: mutated RB gene (retinoblastoma)causes eye tumors to develop
some people may not be born with themutated gene, but a predisposition for the
gene to mutate when exposed toenvironmental carcinogens
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Radiation
UV radiation of sunlight
Radon
nuclear fallout
medical x-rays
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Organic Chemicals
benzene, carbon tetrachloride, vinyl chloride, asbestos fibers,pesticides, dioxins
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Body Burden
Steingraber: 177 different organochlorine residues
detectable in the body of the average middle age man
mutations of p53 can be distinguished by the type ofcarcinogen: cigarette smoke, UV radiation, vinyl chloride
may each derive from a different adduct
some pollutants, I.e. dioxins suppress immune system cells
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Age Specific Exposure
children tend to accumulate higher concentrations than
adults
children have higher metabolic rates, and a lot more handto mouth activity
breastfeeding can transfer large amounts from mother to
infant
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Cancer Process
initiation, promotion, progression
some pollutants can do all three
some do one process at one concentration and others aspollutant load increases
dioxin: promoter at lower concentrations; complete
carcinogen at high concentrations
xenoestrogens (hormone disruptors that mimic estrogen)can be promoters
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Adducts
polycyclic aromatic hydrocarbons (PAHs) caused 2-3x the rate
of adducts in Silesias urban dwellers than in rural populations
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Viruses linked to cancer
hepatitis B: liver cancer
Epstein-Barr: Burkitt lymphoma, nasopharyngeal cancer
human papillomavirus: cervical cancer
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Seven Warning Signs of Cancer
Change in bowel or bladder habits
Asore that does not heal
Unusual bleeding or discharge
Thickening or lump in breast or elsewhere
Indigestion or difficulty in swallowing
Obvious change in wart or mole
Nagging cough or hoarseness
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Routine Screening Tests
Pap Smear
Breast Self Exam
Mammography Testicle Self-Exam
Digital Rectal Exam
Colonoscopy
di i l h i
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Traditional Cancer Therapies
Surgery
Radiation
Chemotherapy
Bone Marrow Transplants: allows higher doses of
radiation or chemotherapy
F C Th i
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Future Cancer Therapies
Vaccines: Melacine against melanoma
Monoclonal Antibodies: bind to cancer cell antigens
(p53) Gene Therapy: use viruses to insert normal p53genes and cause apoptosis
Inhibitory drugs: antiangiogenesis (angiostatin) or anti
metastasis
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A ti i k t
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Actinic keratoses
10% risk of malignant transformation
H t hi AK
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Hypertrophic AKs
C t H
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Cutaneous Horn
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Bowens disease SCC-in-situ
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SCC-in-situ
Also called
Erythroplasiaof Queyrat
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Leukoplakia
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SCC-in-situ
Confirmed by biopsy
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Invasive SCC
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Dysplastic nevi
Precursors for
melanoma
Markers for
melanoma
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Clinical types- MM
Superficial spreading melanoma
Lentigo maligna melanoma
Acral lentiginous melanoma Nodular melanoma
THANK YOU
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THANK YOU
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