Adina Purcareanu, MD

INCIDENCE AND EPIDEMIOLOGY

 The incidence and mortality for gastric cancer have
decreased significantly during the past 7 decades.
 8/100.000; the 7-th cause of death from cancer
 The incidence is higher depending on geographical
areas- Japan, China, Chile and Ireland.
 lower social classes
 age: 75% > 50 years old
 Men/women=2/1
 5-year survival rate is < 10-20 %
 ETIOLOGY
Risk factors:
1. Enviromental
The long-term ingestion of dried, salted, smoked aliments (with high
concentrations of nitrates)
The hypothesis: The nitrates are converted to nitrites by bacteria
- Exogenous sources of bacteria (contaminated foods) have decreased through
better food preservation and refrigeration
- H. Pylori infection?
- Endogenous risk factors: - low gastric acidity
- partial gastrectomy
- atrophic gastritis/ pernicious anemia
- intestinal metaplasia
- long-term administration of H2 receptor antagonists?
- Low intake of fresh fruits and vegetables, A and C vit.; refrigeration
- Lower socioeconomic classes
- Smoking
 ETIOLOGY
2. Genetic factors
- familial gastric cancer- mutation in the E-cadherine
gene
- associated with hereditary nonpolyposis colorectal
cancer
- Blood group A
- GC is three time more often within first degree
relatives
- P53 gene mutation is present in GC, even in early stages
 ETIOLOGY
3. Predisposing conditions
 Gastric ulcer- the cause-and-effect relationship is not
demonstrated; Duodenal ulcer-not involved
 Adenomatous polyps- if they are multiple, bigger than 2
cm and have villous appearance
 Menetrier ‘s disease- polypoid gastric folds
 Blood group A > O
 Chronic atrophic gastritis, with or without intestinal
metaplasia
 Pernicious anemia
 Postgastrectomy, after 15-20 years
 PATHOLOGY
 85%-adenocarcinomas, 15%- nonH lymphomas and
leiomyosarcomas
 Adenocarcinomas
1. Intestinal- in the distal stomach, with ulcerations, preceded by
premalignant lesions
2. Diffuse - involves widespread thickening of the stomach,
especially in the cardia;
- it often affects younger patients
- the prognosis is generally worse
- this form may present as “linitis plastica”, a
nondistensible stomach with the absence of folds and narrowed
lumen; other causes are lymphoma, tuberculosis, syphilis and
amyloidosis.
 PATHOLOGY
 Location: - 37%- proximal third of the stomach
- 30%- antrum
- 20%- midportion of the stomach
- 13%- the entire stomach
 The metastases are independent of the tumor size
 PATHOLOGY
 Early gastric cancer (limited to mucosa and
submucosa) classification:
I. Protrusive
II. Superficial - elevated
- flat
- depressed
III. Excavated
 CLINICAL FEATURES
 In early stages- no symptoms
 Upper abdominal discomfort- vague initially
- postprandial fullness
- steady pain, of high intensity, sometimes with
ulcerative characteristics
 Anorexia, nausea
 Weight loss- late sign
 Vomiting- pylorus T
 Dysphagia- cardia T
 CLINICAL FEATURES
 Hematemesis and melena- rarely; occult bleeding- causing
anemia
 Manifestations of the metastasis:
-spread by direct extension to the adjacent organs: pancreas, liver,
colon and peritoneum
-spread by lymphatics: - to the left supraclavicular lymph nodes –
Virchow’s
- to the intraabdominal lymph nodes
- metastatic nodules to the ovary (Krukenberg`s T)
- periumbilical region (Sister Mary Joseph’s node)
- T palpable on rectal or vaginal examination= Blumer ‘s T
-hematogenous spread: liver, lungs, bones
 CLINICAL FEATURES
 Palpable T mass: late sign
 Cachexia
 Rarely: - migratory thrombophlebitis
- microangiopathic hemolytic anemia
- acanthosis nigricans
 DIAGNOSIS
 Blood tests:
- Iron-deficiency anemia
- microangiopathic hemolytic anemia
- AST, ALT, Alkaline phosphatase (ALP), GGT- Liver
metastasis
- hypoalbuminemia- malnutrition
- CEA, CA 72-4- more useful for postoperative
monitoring
 DIAGNOSIS
 Double contrast radiographic examination- small
lesions and mucosal details
 Upper gastrointestinal endoscopy:
-diagnoses 95-99% of GC
-useful for gastric ulcer (even with benign aspect)- with
biopsy and cytology
- screening method in Japan-the rate of cure is > 80%
for lesions limited to the mucosa or submucosa
 DIAGNOSIS
 Thoracic radiographs
 CT- detects thoracic, abdomen and pelvic invasion
 Echo-endoscopy- the depth of invasion of the stomach
wall and of the lymph nodes
 Paracentesis- peritoneal carcinomatosis
 SURGICAL TREATMENT
 Complete resection of the T and adjacent lymph nodes
- < 1/3 of patients
 Gastrectomy: - subtotal- for distal T- 20 % survival rate
- total- for proximal T + distal
pancreatectomy and splenectomy < 10 % survival rate
 Limited gastric resection is palliative, for bleeding and
obstruction
 Recurrencies continuing for at least 8 years after
surgery
 MEDICAL TREATMENT
 Fluoropyrimidine, oral, postgastrectomy- increases the 3-
year survival rate from 70% to 80%
 Epirubicin + cisplatin + fluorouracil before and after
surgery increases the 5-year survival rate from 23% to 36%
for patients with resection of the gastric tumor
 Fluorouracil and Leucovorin + radiation therapy increases
the survival
 Trastuzumab – increases the survival for HER2 poz. GC
with aproximately 2 months
 Radiation therapy – ineffective; only for palliation
(bleeding, obstruction, pain)
 Jejunal or parenteral nutrition; metabolic correction
 PROGNOSIS
 5-year survival rate is < 10%
 Prognosis factors:
- the location of the T and the involvement of the
lymph nodes; distal GC has better prognosis than the
proximal one
- the depht of the stomach wall invasion
- early GC- 50% survival rate; surgical resection may be
the cure
- mucosal location- endoscopic mucosal resection
 GASTRIC LYMPHOMA
 < 15 % of GC
 < 2 % of lymphomas; the most frequent extranodal
location
 The frequency has increased during the past 20 years
 At younger patients; men> women
 DIAGNOSIS
 Clinically it can`t be distinguish from adenocarcinoma
 Contrast radiographs- thickened folds with ulcerations
 UGE with biopsy (superficial biopsies may miss the
deeper lymphoid infiltrate)
- bulky ulcerated T in the antrum or corpus
- diffuse process spreading throughout the submucosa
and even extending to the duodenum
 DIAGNOSIS
 AP-the majority of the lymphoid T are non-Hodgkin`s
lymphomas of B cell origin

 Histologically: - well-differentiated, superficial T- MALT

(mucosa-associated lymphoma tissue)
- large-cell lymphomas
 H. Pylori increases the risk for gastric lymphoma in general and
MALT lymphomas in particular

 CT for the thorax, abdomen and pelvis

 Bone marrow biopsy

 First spread is on local lymph nodes

 TREATMENT
 The prognosis of the patient with gastric lymphoma after
the treatment is better than for the patient with ADK- the
importance of the differential diagnosis
 H. Pylori treatment- has led to regression of 50% of the
patients with MALT lymphomas
 Subtotal gastrectomy followed by chemotherapy- 5-year
survival rates of 40-60% in patients with localized high-
grade lymphomas.
 It has been proposed chemotherapy alone for patients with
nodal involvement
 Radiation therapy- is not defined
 GASTRIC SARCOMA
 1-3 % of GC
 Leiomyosarcoma- the most frequent
 The most frequently it affects the anterior and
posterior walls of the gastric fundus and often ulcerate
and bleed; intramural mass with a central ulceration
 Clinical features- bleeding and palpable mass
 Liver, pulmonary and nodal metastasis
 TREATMENT
 Of choice- surgical resection; 5-year survival rate of 50
%
 Chemotherapy is given to patients with metastatic
disease
GIST
 GI stromal tumor
 Associated with C-kit gene mutation, like the acute
and chronic myeloid leukemia and Crohn’s disease
 surgical resection
 are unresponsive to conventional chemotherapy
 50 % are responsive to imatinib(selective inhibitor of
the C-kit tyrosine kinase), like CML, or sunitinib-
increases the survival rate
 Leiomyosarcomas and GISTs appear benign on
histologic examination but may behave in a malignant
fashion
-not metastasize to lymph nodes
-spread to the liver and lungs