Description of cancer of the stomach

1. Neoplasms of the Stomach
MUNYAGA BYANJO
ONEN JACOB JABWELI

2. Epidemiology
5th most common malignancy worldwide (1,033,701 new
cases in 2018)
The second cause of cancer related death (782,685 deaths in
2018).
Cumulative incidence rate up to and including 74 years is
1.39% globally, 0.46% in Sub-Saharan Africa.

3. • 31,148 new cases and 28,707 death occurred in africa in
2018, with 9,215 new cases and 8,908 deaths of those
occurred in East Africa.(Globocan 2018)
• In Uganda, gastric cancer is 2.7-3% of total cancers, majorly
affects males. (Kampala cancer registry report 2009)
• Male incidence 53/100,000 and female incidence
28/100,000

4. • In western uganda, 2nd most common cancer 12% of all cancers in
males and 6% of all cancers in females (parkin et al, 2003)
• Gastric cancer prevalent in tribes inhabiting volcanic areas of south
western uganda (ibingira CB, 2001)
• Approximately 200 were admitted confirmed cases in UCI in 2018.

6. Introduction
• A trend of steady decline in gastric cancer incidence rates has been
observed globally.
• Time trends for registries in Kampala (Wabinga et al 2014), Harare
(Chokunonga et al 2013), and Bamako(Mali) indicate no change in
incidence over past 20 years
• H.pylori most important riskfactor for non-cardia gastric cancers
(IARC, 2012)

7. • 95% are adenocarcinoma, 5% are the rest.
• The disease becomes symptomatic in an advanced stage. Five-year
survival rate is relatively good only in Japan, where it reaches 90%.
• May have malignant tumors from adjacent organs invade the stomach
by direct extension (e.g., colon or pancreas).

8. Etiology
• The etiologic influence may reside more in environmental than
ethnicity factor
• Diets rich in salt, smoked or poorly preserved foods, nitrates, nitrites,
and secondary amines to be associated with an increased risk of
gastric cancer.
• In contrast, diets rich in fruits and vegetables may be associated with
a reduced risk of cancer through their anti-oxidant effects.

9. Etiology
Prolonged consumption of salty foods
Atrophic gastritis with alteration in
gastric environment
Generation of carcinogenic N-nitroso
compounds

10. Risk factors
• Cigarette smokers have a 2 to 3 times increased risk of proximal
gastric cancer.
• Association with H. pylori infection which induces changes in the
gastric mucosa. Increases risk 3x
• Others factors include chronic atrophic gastritis, gastric polyps, low
socioeconomic status, and obesity.
• EBV: 10% gastric adenocarcinomas carry EBV, late step in gastric
carcinogenesis

14. Pathology
• May be intestinal or diffuse
• Intestinal-type adenocarcinomas typically grow along broad cohesive
fronts to form either an exophytic mass or an ulcerated tumor.
• The neoplastic cells often contain apical mucin vacuoles, and
abundant mucin may be present in gland lumina.

15. Pathology
Diffuse gastric cancers:
Display an infiltrative growth pattern
Are composed of discohesive cells with large mucin vacuoles that
expand the cytoplasm and push the nucleus to the periphery, creating
a signet ring cell morphology.

16. These cells permeate the mucosa and stomach wall individually or in
small clusters.
Evokes a desmoplastic reaction that stiffens the gastric wall and may
cause diffuse rugal flattening and a rigid, thickened wall that imparts a
“leather bottle” appearance termed linitis plastica.

18. Classification of gastric cancer
Sporadic gastric cancer
• The majority of GC occurs sporadically and mainly affects people over
the age of 45 years.
• They are commonly caused by coincidence of many environmental
factors.
• They occur at the age of 60–80 years, and males are two times more
often affected than females, particularly in high-risk countries

19. Early onset gastric cancer
• EOGC is defined as GC before the age of 45 years and encompasses
about 10% of GCs.
• In EOGCs, genetic factors seem to play the causal role.
• These cancers are often multifocal, diffuse, and are more frequently
observed in females, probably because of hormonal factors.

20. Gastric stump cancer
• occurs in the gastric remnant at least 5 years after the surgery for
peptic ulcer.
• GSC represents from 1.1% to 7% of all GCs and males are more prone
to them than woman.
• Gastrectomy is a well-established risk factor for GSC increases risk by
4.
• EBV infection is more often in gastric remnants than in intact
stomachs.

21. Hereditary diffuse gastric cancer (HDGC)
• Contributes 1%–3% of all GCs
• They result from inherited syndromes, one of which are germline
mutations in the CDH1 gene that encodes E-cadherin.
• These are autosomal dominant conditions that cause diffuse, poorly
differentiated GC, which infiltrates into stomach wall and causes
thickening of the wall without forming a distinct mass.

23. Gross morphology
• There are four gross forms of gastric cancer: polypoid, fungating,
ulcerative and scirrhous.
• In the first two, the bulk of the tumor mass is intraluminal, both being
ulcerated.
• In the latter two gross subtypes, the bulk of the tumor mass is in the
wall of the stomach.
• Ulcerative tumors are self-descriptive; scirrhous tumors infiltrate the
entire thickness of the stomach and cover a very large surface area.

25. Pathological types of early gastric cancer

26. Clinical presentation
• Anorexia
• Nausea and vomiting ~ 40%
• Early satiety
• Distaste for meat
• Weakness and dysphagia
• Abdominal pain ~ 60%
• Weight loss ~ 50%
• Anameia ~ 40%
• Palpable Abdominal pain

27. Staging

30. Treatment
• Radical subtotal gastrectomy (distal 75% of the stomach removed)
• Negative margin of 5cm
• Reconstruction is by a billroth ii gastrojejunostomy
• Chemotherapy, either alone as a perioperative treatment, or in
combination with radiation therapy in an adjuvant setting, improves
the clinical outcome for patients with resectable tumors.

31. Role of chemotherapy
• Agents used: 5-FU, cisplatin, doxorubicin, methotrexate, taxanes,
camptothecin
• Triple combination chemotherapy associated with better prognosis
• Targeted molecular agents: transtuzumab
• Human molecular Ab rective against the extracellular domain of HER2

32. MoA tanstuzumab
• Blocking of HER-2 receptor cleavage and inhibitingdimerization
• Increasing receptor destruction by endocytosis
• Inhibiting intracellular pathway signaling such as phosphoinositide 3-
kinase signaling; may indirectly modulate
proangiogenic and antiangiogenic factors, such as vascular endothelial
growth factor production
• Inducing G1 phase arrest by inducing the cyclindependent kinase
inhibitor, p27 Kip1

33. Prognosis
• Depends on stage, tumor size, location
• 5 year survival is 75%, 50% and 25% for stage 1, 2 and 3 respectively
for resected adenocarcinoma.
• Median survival of 24 months (20–30% 5-year survival) in tumors
resected with curative intent,
• A median survival of 8.1 month after palliative procedures, and a
median survival of only 5.4 months for advanced disease without an
operation.

34. References:
• Bryan J. Dicken, MD,* David L. Bigam et. al. Gastric Adenocarcinoma,
Review and Considerations for Future Directions, 2005
• Scwartz principles of surgery, 10th edition.
• Robbin textbook of pathology, 9th edition
• Globocan 2018