Brief intro about ca stomach

1. GASTRIC ADENOCARCINOMA
• Most common malignancy
• Clinical - resemble chronic gastritis---
dyspepsia, dysphagia, nausea, constitutional,
anemia
• Discovered at late stage

2. Pathogenesis
• Age >50 , more on men, Blood group A
• Japan, south America, east Europe
Risk factors :
• Mutations - loss of E-cadherin function seems to
be a key step in the development of diffuse
gastric cancer; patients with FAP who have germ
line mutations in adenomatous polyposis coli
(APC) genes have an increased risk for
development of intestinal-type gastric cancer;
Sporadic tumors show mutations in b-catenin,
MSI, p16 and p53 genes.

3. Pathogenesis
• H pylori - increased production of proinflammatory
proteins, such as interleukin-1β (IL-1β) and tumor
necrosis factor (TNF).
• Epstein-Barr virus (EBV) - 10% of gastric
adenocarcinomas; tend to occur in the proximal
stomach and most commonly have a diffuse
morphology with a marked lymphocytic infiltrate.
• Nitrosamine/benzo(a)pyrene-salted and smoked meat
and pickled vegetables
• Achlorydria
• Chronic gastritis – multifocal with intestinal metaplasia
and atrophy

4. Prognosis
• Depth of invasion
• Extent of nodal and distant metastasis
• Virchows node- mets to supraclavicular node
• Krukenberg tumor- spread to both ovaries in
females

5. INTESTINAL TYPE
• Polypoid /fungating
• Can become ulcerated -
irregular necrotic base and
firm rolled elevated raised
margins
• Association with H pylori
• Decrease in incidence

6. DIFFUSE TYPE
• Linitis plastica, leather
bottle stomach
• Diffuse infiltration of
tumor cells (signet
ring) with extensive
fibrosis

7. GASTRINTESTINAL STROMAL TUMOR
• Most common mesenchymal tumor of GIT
• More than half occur in stomach
• Clinical- more in males, around 60 years.
• Mass effects or mucosal ulceration, such as
intestinal obstruction or gastrointestinal
bleeding.

8. Pathogenesis
• Arise from interstitial cells of cajal (located in musclaris propria,
pacemakers of peristalsis)
• Mutation in genes encoding tyrosine kinase receptor-
 c KIT
 PDGFRA
• Prognosis correlates with tumor size, mitotic index, and location,
with gastric GISTs being somewhat less aggressive than those
arising in the small intestine.
• Recurrence or metastasis is rare for gastric GISTs less than 5 cm
in diameter but common for mitotically active tumors larger
than 10 cm.
• Treatment- surgical resection , Imatinib

9. Morphology
• Solitary ,well
circumscribed
fleshy masses
covered by
mucosa
• Microscopy -
spindle cell
type, epithelioid
type, mixed
• IHC - C-KIT

10. NEUROENDOCRINE (CARCINOID)
TUMORS
• Neoplasm arising from neuroendocrine cells
• Indolent course - well differentiated
• Throughout GIT- most commonly small intestine (40%),
appendix than stomach
• Maybe associated with endocrine cell hyperplasia,
chronic atrophic gastritis, Zollinger Ellison syndrome
• Clinical- flushing , wheezing, diarrhea, bronchospasm,
colicky abdominal pain, and right-sided cardiac valvular
fibrosis.

11. MORPHOLOGY
• Gross-polypoid lesion,
• Neuroendocrine cells-
salt and pepper
chromatin
• Round uniform nuclei
• Electron microscopy-
neurosecretory
granules

12. Prognostic factor- Location
• Foregut carcinoids - stomach, duodenum---
rarely mets , cured with resection ,
gastrinomas associated with PPI.
• Midgut carcinoids - jejunum, ileum-----
multiple, aggressive (size, depth of invasion,
necrosis and mitosis).
• Hindgut carcinoids- appendix, colon-----
incidental

13. LYMPHOMAS
Extranodal lymphomas- particularly stomach
• B cell lymphoma
• Extranodal marginal B zone lymphomas-
MALTOMAS
• Diffuse large B cell lymphoma
• T cell lymphoma

14. MALTOMA
• Lymphomas of mucosa associated lymphoid
tissue
• Low grade lymphoma
• Can transform into highly aggressive tumors
• Occur in background of chronic H pylori
associated gastritis
• Clinical- dyspepsia, epigastric pain,
constitutional symptoms, hematemesis,
melena

15. Pathogenesis
• Arise at site of chronic inflammation (H pylori infection)
or MALT (Peyers patch in intestine)
• H pylori gastritis - eradication with antibiotics induces
remission
• Inflammation leads to activation of lymphocytes
leading to polyclonal B cell hyperplasia and emergence
of monoclonal B cell neoplasm
• Translocations: T(11;18)(q21:q21) , t(1:14), t(11:14)
Failure - transformation to large cell lymphoma, invasion
of muscularis prorpria and lymph node mets

16. Morphology