Neoplasms of the Gastrointestinal Tract

Neoplasms of the Gastrointestinal Tract

Dr. M JeffersConsultant HistopathologistAMNCH, Tallaght

AMNCH Tallaght

Objectives: GI tumour pathology

tumour nomenclature and classification

tumour aetiology and pathogenesisprecursor lesionsmechanisms of carcinogenesis in different tissuespotential points for prevention / modification

tumour growth and behaviourinvasionmetastasis

tumour stagingstaging systemsprognostic factors

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Useful links

http://medstat.med.utah.edu/WebPath/webpath.html

www.bmj.com : collected resources

ABC of colorectal cancerABC of the upper gastrointestinal tract: cancer of the stomach and pancreas

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Neoplasms

Definition

Epidemiology, Aetiology, Pathogenesis

Morphology: Gross / Microscopic

Clinical presentation and outcome

Prognosis

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Nomenclature and Classification

Nomenclature / Classification by histogenesis:

Epithelial

Mesenchymal

Neuroendocrine

Haematolymphoid

Melanocytic

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Epithelial tumours:

Benign: “adenoma”

Malignant: “carcinoma”

Adenocarcinoma Squamous carcinoma Small cell carcinoma

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Neuroendocrine tumours:

Benign: “carcinoid”

Malignant: neuroendocrine carcinomasmall cell carcinoma

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Mesenchymal tumours:

Benign: (tissue)oma lipoma, leiomyoma etc

Malignant: (tissue)sarcoma liposarcoma, leiomyoma etc

Gastrointestinal stromal tumour (GIST): benignlow malignant potentialmalignant

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Haematolymphoid tumours:

Bone marrow neoplasm (+/- circulating cells): leukaemia

Lymph node / extranodal lymphoid cell tumour: lymphoma

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Concepts:

Carcinogenesis: Metaplasia/Dysplasia/Carcinoma sequenceAdenoma/Carcinoma sequence

Differentiation

Invasion and Metastasis

Tumour staging

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Tumour Aetiology and Pathogenesis: Carcinogenesis

Various mechanisms operative in carcinogenesis in the GI tract:

Intraepithelial neoplasia – Dysplasia – Carcinoma

Metaplasia – Dysplasia - Carcinoma

Adenoma - Carcinoma sequence

Replicator error phenotype

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Intraepithelial neoplasia – carcinoma sequence

Multistage process of carcinogenesis from

normal through low grade intra-epithelial neoplasia (dysplasia) (RR 2.2) through high grade intra-epithelial neoplasia (dysplasia) (RR >60) to invasive carcinoma.

Progressive development of architectural and cytological abnormalityProgressive increase in relative risk of invasive carcinoma

Useful model is squamous cell carcinoma of oesophagus.

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Intraepithelial neoplasia – carcinoma sequence: Oesophageal cancer

Morphologic abnormality in dysplasia –carcinoma sequence in oesophageal mucosa reflects underlying genetic abnormality.

p53 mutationlow grade

LOH 3p14 (FHIT) fragile histidine triad, tumour suppressor gene

Cyclin D1 overexpression (11q13), 3p21 LOH

C-myc, EGFR, HST1 overexpression invasive carcinoma

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Intraepithelial neoplasia – carcinoma sequence

Normal oesophageal squamous mucosa

High grade squamous dysplasia (carcinoma in-situ)

Invasive squamous cell carcinoma

p53 mutation FHIT LOH CYD1 c-myc, EGFR, HST1

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Metaplasia – Dysplasia – Carcinoma Sequence

Multistage process of carcinogenesis from

Normal throughMetaplastic columnar epithelium throughDysplasia in metaplastic epithelium

low gradehigh grade to

Invasive carcinoma

Useful model is adenocarcinoma of oesophagus

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Metaplasia – Dysplasia – Carcinoma sequence:Oesophageal cancer

Barrett’s oesophagus = columnar lined oesophagus

Replacement of the squamous lining of the distal oesophagus by glandular mucosa in response to injury, most frequently gastro-oesophageal refluxmetaplasia to gastric and intestinal type epithelium

Stepwise progression of dysplasia in metaplastic epithelium leads to invasive malignancy: architectural and cytological abnormalities develop.

Morphologic changes reflect underlying molecular genetic / cell cyle regulatory abnormalities

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Normal

MetaplasiaFHIT alterations, CDKN2A hypermethylation

Dysplasiarab11 abnormalities

Low gradeKi67 abnormality

High grade APC mutation

p53 mutation (different to scc)

Invasive carcinoma c-erbB2, EGFR

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Normal oesophageal squamous mucosaBarrett’s oesophagus: metaplastic columnar and intestinal mucosa

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Barrett’s oesophagus: low grade dysplasia

Barrett’s oesophagus: high grade dysplasia

Invasive adenocarcinoma

FHIT Ki67 p53 APC

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The metaplasia dysplasia sequence: significance

Intestinal metaplasia in the oesophagus is a marker of increased adenocarcinoma risk

Risk of carcinoma is greatest with high grade dysplasia: concurrent carcinoma in up to 50%

Many cases of high grade dysplasia will progress to invasive carcinoma over time

Diagnosis of high grade dysplasia: rebiopsy to exclude invasion consider surgery

Diagnosis of metaplasia: treat underlying conditions (GORD)surveillance endoscopy to identify dysplasiaaiming to prevent cancers / detect cancer early

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Metaplasia – Dysplasia – Carcinoma sequence:Gastric cancer

Chronic atrophic gastritis is a major risk factor for gastric carcinoma (intestinal type)

Risk of malignant transformation is strongly linked to intestinal metaplasia and intra-epithelial neoplasia (dysplasia)

Variety of processes may lead to atrophic gastritis:Helicobacter gastritisAuto-immune gastritis

Metaplasia – dysplasia sequence acts as a final common pathway in development of malignancy

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H Pylori infection

Gastritis

iNOS expression

NO

Cell damage (DNA, lipids, mitochondria etc)

Apoptosis

Atrophic gastritis

Ascorbic acid

Nitrate reductase

Nitrite Diet

Acid

N2O3

Nitrosamines

Mutation

Cancer

Repair

Metaplasia / dysplasia

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Metaplasia – Dysplasia – Carcinoma sequence:Gastric cancer

Chronic gastritis

Intestinal metaplasia

Dysplasia

low grade

high grade

Invasive carcinoma

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Metaplasia – dysplasia - carcinoma sequence in the stomach

Stomach: normalStomach: chronic gastritis

Stomach: atrophy and intestinal metaplasia

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Metaplasia – dysplasia - carcinoma sequence in the stomach

Stomach: low grade dysplasia Stomach: high grade dysplasia

Stomach: invasive adenocarcinoma

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The metaplasia dysplasia sequence: significance

Most intestinal type gastric cancers develop on a background of atrophy, metaplasia and dysplasia.

Predisposing factors for atrophy and metaplasia are known:chronic HP gastritis, auto-immune gastritis etc.

Treatment of predisposing conditions, endoscopic surveillance of patients with documented metaplasia: strategies to reduce risk, detect cancer early.

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Colorectal carcinogenesis: the adenoma – carcinoma sequence

Various epidemiological associations in colorectal carcinoma point to the important role of the adenoma as the precursor lesion of many cancers

Morphological progression in colorectal carcinoma:

Aberrant crypt focus dysplastic ACF with APC mutation inactivation

Adenoma proto-oncogene activation: c-myc, ras

low grade dysplasia suppressor gene inactivation: p53, p21, bax

high grade dysplasiaother abnormalities: BRCA, DCC, E-cad

Carcinoma

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Normal Epithelium

Early Adenoma

Intermediate

Adenoma

Late

Adenoma

Carcinoma

CarcinomaMSI +

Metastasis

Methylation Defect

APC

K-Ras Smad4 p53

Mismatch repair defectTGF, BAX

Genetic Model for Sporadic Colorectal Carcinogenesis

??

??

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Adenomatous polyps of the colon

Neoplastic polyps, precursors of carcinoma

Architectural patterns:Tubular/Villous/Tubulovillous

Gross presentation:sessile/pedunculated/flat adenoma

Risk of malignancy size (ras), architecture, dysplasia

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Colon: tubular adenoma

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normal epithelium adenomatous epithelium

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Colon: villous adenoma

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Polyposis syndromes

Sydromes characterised by multiple polyps in colorectum +/- elsewhere in GIT

FAP: 5q21 defect, multiple polyps, 100% lifetime risk of carcinoma

HNPCC: MSH gene defect, fewer polyps, typical pattern of tumours

Gardner: variant of FAP with skin and other lesions

Turcot: association with CNS neoplasms

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Table 1. Intestinal polyposis syndromes Location Location of Location of Syndrome Inheritance Type(s) of polyp of polyp Gl cancer extraintestinal tumorsFamilial polyposis AD Adenoma, FGP C, SI, ST C, SI Nonecoli (familial adenomatous polyposis) Gardner’s AD Adenoma; FGP, C, SI, ST C, SI Lipoma; fibroma; desmoid lymphoid tumor; dental cysts; osteoma; carcinoma of thyroid and adrenal glandsTurcot’s* AD Adenoma C C Central nervous system tumorsPeutz-Jeghers AD Hamartoma C,SI,ST C,SI,ST Cancers of the breast, ovary, uterus, and testis Juvenile polyposis AD Juvenile C,SI,ST C,SI,ST None(one-third of cases) Cowden’s AD Hamartoma; C,SI None Facial trichilemomas; inflammatory; oral mucosal papillomas;

ganglioneuroma; carcinoma of thyroid lipoma; lymphoid gland and breastCronkite-Canada None Juvenile-like C,SI,ST Colon (rare) None

Attenuated AD Adenoma; FGP C,SI,ST C,SI,ST Nonefamilial polyposis coli** Hereditary flat AD Adenoma; FGP C,SI,ST C,SI,ST NoneAdenoma syndrome** Muir Torre syndrome AD Adenoma C C Skin cancer: basal cell;

squamous cell; sebaceous carcinomaHereditary mixed AD Adenoma; juvenile; C C Nonepolyposis syndrome hyperplastic GI, gastrointestinal, AD, autosomal dominant, FGP, fundic gland polyp; C, colon; SI, small intestine; ST, stomach. *Some cases of Turcot’s syndrome have mutations in APC gene, Some cases of Turcot’s syndrome have germline mutations in mismatch repair genes (hMLH1 and hPMS2). **Attenuated familial polyposis coli and hereditary flat adenoma syndrome most likely are the same disorder, but they are listed separately in this table. Attenuated familial polyposis coli and hereditary flat adenoma syndrome are considered variants of familial polyposis coli.

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Familial adenomatous polyposis (FAP)

Autosomal dominant condition characterised by numerous adenomatous polyps and high risk of progression to adenocarcinoma

Germline mutation in APC gene (5q21-22) which encodes a 2843 aa polypeptide which acts as a negative regulator in the Wnt signalling pathway, regulates cellular -catenin concentration

Lack of functional APC leads to accumulation of -catenin and consititutive expression of c-myc and cyclin D1

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Colon: familial adenomatous polyposis

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Adenoma carcinoma sequence: significance and implications

Mechanism underlying most colorectal carcinomas

Identifiable precursor lesions in many cases: early detection of precursor lesions has obvious implications for early treatment and prevention of invasive disease

Identification of families with germ-line mutations and significant polyposis syndromes offers significant preventive opportunities

Tumour pathogenesis has direct implications on cancer management and prevention

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Colorectal carcinogenesis: the mismatch repair defect pathway

Mechanism of carcinogenesis distinct from the adenoma – carcinoma sequence

Tumours characterised by extensive nucleotide insertions / deletions in repeated sequences in tumour DNA: microsatellite instability (MSI) / DNA replication error (RER)

Tumours with MSI are classified as MSI high-frequency (MSI-H) or MSI low frequency (MSI-L)

These tumours arise through defects in the DNA mismatch repair mechanism, defects which may be sporadic or inherited

Some sporadic tumours are MSI-H but most MSI-H tumours characteristic of hereditary non-polyposis colorectal carcinoma (HNPCC)

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HNPCC

HNPCC: a syndrome characterised by inherited defects in DNA repair due to germline mutations of the relevant genes: (hMLH1, hMSH2)

High frequency of colorectal carcinomaExtracolonic tumours in endometrium, stomach, ovary, brain, skin, small

bowel

Criteria for classification as HNPCC: Amsterdam criteria (+ revisions)

Classical tumour characteristics: right sided, large, mucinous, low stage

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Hereditary Non-polyposis Colorectal Cancer

Criteria:At least 3 relatives with a HNPCC associated cancer (colorectum/endometrium/small bowel/ureter/renal pelvis)

Ones should be first degree relative of other two

At least 2 successive generations involved

At least one tumour diagnosed before 50 yrs of age

Familial adenomatous polyposis should be excluded

Tumours should be verified by histopathological examination

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MSI in colorectal cancer: diagnosis

hMSH2: normal hMSH2: tumour

Normal tissue: hMSH2 expression Loss of expression in MSI-H tumour

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Replicator error phenotype: implications

Identification of MSI-H tumours confers a high probability of an inherited cancer

Cancers can be screened for MSI status, confirmation of germ-line status required for definition of syndrome

Careful family history combined with tumour characteristics can identify at-risk groups

Early intervention and prevention opportunities

Tumour pathogenesis impacts directly on patient management and prognosis.

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Carcinogenesis: review of mechanisms

Various mechanisms operative in carcinogenesis in the GI tract:

Intraepithelial neoplasia – Dysplasia – Carcinoma

Metaplasia – Dysplasia - Carcinoma

Adenoma - Carcinoma sequence

Replicator error phenotype

Various mechanisms implicated at different sites

Significance in terms of identification of precursor lesions, treatment and prevention of cancer

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Differentiation

Differentiation refers to the degree of maturation of tumour cells / tissues:

what cell type / tissue type does the tumour grow in ?

how closely does the tumour reproduce normal tissue architecture ?

Tumours are described as: well differentiatedmoderately differentiatedpoorly differentiated

Differentiation is closely related to tumour grade:

well differentiated – low gradepoorly differentiated – high grade

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Differentiation: colorectal carcinoma

well differentiated moderately differentiated poorly differentiated

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Classification of tumours:

Anatomical Location

Origin (Primary/Secondary)

Behaviour (benign/uncertain/malignant)

Histogenesis (epithelial/stromal/lymphoid etc)

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Tumours of the oesophagus

Benign tumours rare:

Leiomyoma

Most are malignant and most are carcinomas

Squamous cell carcinomaAdenocarcinoma

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Oesophageal carcinoma

Approx 6% of GIT cancers

1996 Irish Cancer Registry data:

299 cases (1.4% of all cancers)

303 deaths (4.1% of all cancer deaths)

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Histological types:

Squamous cell carcinomaAdenocarcinoma (a/w Barrett’s oesophagus)Others

Relative proportion of squamous and adenocarcinoma varies with geography

Adenocarcinoma increasing incidence

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Squamous carcinoma:

Alcohol, Tobacco, Food, HPVArise on background of dysplasia / in-situ carcinomaVarying differentiation

well - poorly differentiated

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Normal Oesphagus

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Oesophageal squamous carcinoma

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Squamous cell carcinoma

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Adenocarcinoma:

Majority arise on a background of Barrett’s oesophagus.Metaplasia - Dysplasia - Carcinoma sequenceSequential acquisition of genetic abnormalities, oncogene activation,

TSG inactivation Majority are intestinal type adenocarcinoma

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Invasion through submucosa, muscularis and into soft tissueMetastasis to regional nodes, distant sites

Most are advanced at diagnosis5 year survival is poor (<30%)Early diagnosis improves outcome

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Tumours of the stomach

Benign tumours are rare:

Leiomyomas etc

Malignant tumours:

carcinoma >> lymphoma, stromal tumours, carcinoid tumours

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Gastric carcinoma

Irish Cancer Registry Data 1996:

482 cases (2.3% of total cancers)399 deaths (5.4% of total cancer deaths)

Male : female 1.5:1

18 lymphomas in same time period

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Gastric carcinoma

Pathogenesis:

Chronic gastritis - metaplasia - dysplasia(H Pylori)

Dietary factors, smokingGenetic factors (HNPCC)

Dysplasia is a final common pathway in intestinal type tumours

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Gastric carcinoma

Tumour pathology: 2 major types:

Intestinal: Bulky masses / ulcers, glandular pattern

Diffuse: infiltrative lesions, “signet-ring” cells

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Gastric tumour

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Gastric cancer: Linitis Plastica

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Normal stomach mucosa

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Gastric adenocarcinoma: diffuse type

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Gastric adenocarcinoma: signet ring cells

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Gastric carcinoma

Late presentation is typical

6% present in stage I, 30% stage IV(of those staged)

Prognosis is poor:

Cumulative probability of survival34% @ 1yr20% @5yrs

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Gastric carcinoma

Importance of Pathologic Staging:

Early gastric carcinoma is disease limited to mucosa and submucosa, irrespective of nodal involvement

5ys is >90% with surgical resection

Advanced gastric carcinoma is disease which invades the muscularis propria

5ys is <20% regardless of treatment

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Gastric carcinoma

Patterns of disease spread:

Direct invasion: stomach wall, adjacent structures

local/regional/distant nodal metastases: lesser/greater curve, porta hepatis

haematogenous dissemination: liver, lungs

peritoneal spread (Krukenberg tumour of ovaries)

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Adenocarcinoma of the oesophago-gastric junction

Adenocarcinoma which crosses the junction of oesophagus and stomach, regardless of where the tumour bulk lies

(entirely above ogj: oesophageal carcinoma entirely below ogj: gastric carcinoma)

Typically a tumour of older malesIncreasing in frequency (gastric carcinoma decreasing)

Principal predisposing factor is GERD (not diet or HP gastritis)

Typically present late

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Other tumours of the stomach

Lymphoma:Low grade B cell MALT lymphoma

clonal B cell process related to chronic H Pylori infectionHigh grade B cell lymphoma

Carcinoid tumours

Stromal neoplasmstumours of muscle/nerve/vascular etc phenotype

Metastases

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Stomach: large B cell lymphoma

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Carcinoid tumours of stomach

1. Atrophic gastritis / Pernicious anaemiahypochlorhydria, antral G cell hyperplasia, Gastrin ,

ECL cell

2. Sporadic (G cell or ECL) not a/w hypochlorhdyria

3. Fundic ECL tumours in patients with Zollinger-Ellison syndrome

4. Poorly differentiated small cell carcinoma

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Tumours of the small intestine

Small bowel: 75% of GIT, 6% of GIT tumours

Adenomas:majority occur in region of ampulla of Vaterprecursor of carcinoma in this location

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Tumours of the small intestine: Carcinoma

Adenocarcinoma:

Most occur in duodenum and jejunum

Most probably arise from precursor adenoma

Typical intestinal type adenocarcinomas

May obstruct/perforate/bleed/spread

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Ampullary carcinoma

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Tumours of the small intestine: Carcinoid Tumour

Carcinoid tumour:

origin from endocrine (APUD/Kultchitsky cells)

cells are neuroendocrine type, contain neurosecretory granules

may produce hormone and cause carcinoid syndrome

behaviour depends on depth of infiltration intra-mural: good prognosis, peritoneal involvement: poor prognosis

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Small intestinal carcinoid tumour

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Carcinoid tumour

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Tumours of the small intestine: Lymphoma

Lymphoma:

B cell lymphoma may be of MALT type or non-MALTT cell lymphoma associated with enteropathy (coeliac disease)

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Tumours of the small intestine: Stromal tumours

Stromal tumours:

Tumours derived from mesenchymal structures: muscle ,nerve, interstitial cells etc.

Spectrum from benign-indeterminate-malignantUsually present as bulky masses with perforation / obstruction /

haemorrhageCriteria for malignancy include size, necrosis, proliferation

Most are Gastrointestinal Stromal Tumours (GIST)probably of interstitial cell originc-kit (CD117) mutation

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Tumours of the appendix

Carcinoid tumour:

small, often at tip of appendixtypical carcinoid / goblet cell carcinoid

Mucinous neoplasms:

mucinous cystadenomamucinous cystadenocarcinomaMay be associated with Pseudomyxoma Peritoneii

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Colorectal Tumours

Polyps:

Hyperplastic (metaplastic)Inflammatory, Juvenile, Hamartomatous

AdenomatousSporadic / Hereditary syndromes

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Colorectal cancer

Risk factors / associations:Geography: industrialised societiesObesity, inactivityDiet: meat and refined carbohydratesfamily historyadenomatous polyps (sporadic/familial syndromes)ulcerative colitis

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Colorectal Carcinoma

>70% arise from adenomasadenoma incidence is ~ 30 -40%immediate family of affected patient: risk x 2-3

~ 2% arise on a background of ulcerative colitis

different genetic pathways to neoplasia:(1) adenoma - carcinoma sequence(2) hereditary non-polyposis mechanism(3) UC associated neoplasia

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Adenomatous polyps of the colon

Neoplastic polyps, precursors of carcinoma

Architectural patterns:Tubular/Villous/Tubulovillous

Gross presentation:sessile/pedunculated/flat adenoma

Risk of malignancy size (ras), architecture, dysplasia

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Colon: tubular adenoma

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Colon: villous adenoma

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Colitis-associated neoplasia

UC increases risk x 2-8

Risk increased with - duration of disease - extent of disease

- presence of dysplasia

neoplasm evolves from dysplasia rather than adenoma

bcl-2 overexpression less frequent in UCAN

APC gene mutations much less frequent in UCAN

E-cadherin mutations more frequent in UCAN

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Colorectal carcinoma: Pathology

Virtually all are adenocarcinomas

Irish Cancer Registry 1996:

1784 cases (8.6% of all cancers, largest group apart from skin cancer), close to European average

Crude incidence 40% > in malesAge standardised incidence 75%> in males

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Colorectal carcinoma

Left > right side

Left side tend to be annular obstructing lesionsRight side tend to be polypoid exophytic

Intestinal type adenocarcinomas, range of differentiation: well- moderate –poor

+/- mucinous, neuroendocrine differentiation

Mucinous differentiation more common in right sided tumours, HNPCC association

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Colon: carcinoma

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Colon: carcinoma

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Colon: adenocarcinoma

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Infiltrate into and through wallmetastasize to regional nodesdisseminate through blood to liver, distant sites

prognosis is primarily dependent on stageStaging: Dukes’ A B C

Dukes’ variantsTNM

Accurate staging depends on pathological examination of resected specimen in conjunction with clinical and radiological information

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Dukes’ A

Dukes’ B

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Dukes’ C

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Stage at diagnosis:Stage 1: <20%Stage 4 >20%

Cumulative survival probability: 1 yr 69%, 3yrs 51%

1yr: stage 1 90%, stage 4 30%3yr: stage 1 80%, stage 4 10%

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Objectives: GI tumour pathology

tumour nomenclature and classification

tumour aetiology and pathogenesisprecursor lesionsmechanisms of carcinogenesis in different tissuespotential points for prevention / modification

tumour growth and behaviourinvasionmetastasis

tumour stagingstaging systemsprognostic factors

Documents

Neoplasms of the Gastrointestinal Tract