1. Carcinoma
Stomach
Professor AMSM Sharfuzzaman
Professor of Surgery
Sher-e-Bangla Medical College
January 8, 2013 DR. RUBEL,SBMC 1

2. Introduction
Gastric cancer is the second most common cause of cancer-related
death in the world. Many Asian countries, including Korea China,
Taiwan, and Japan, have very high rates of gastric cancer.
Gastric cancer was the leading cause of cancer deaths in men and
the third leading cause of cancer deaths in women in the early 1940s.
Gastric cancer remains a difficult disease to cure in Western
countries, primarily because most patients present with advanced
disease. Even patients who present in the most favorable condition and
who undergo curative surgical resection often die of recurrent disease.
January 8, 2013 DR. RUBEL,SBMC 2

3. Introduction-contd.
Adenocarcinoma of the stomach is the second most common cancer
worldwide. In 2001, stomach cancer affected 850,000 people, of which
522,000 men and 328,000 women died of stomach cancer.
Tremendous geographic variation exists in the incidence of this disease
around the world. The highest death rates are recorded in Chile, Japan,
South America, and the former Soviet Union. Over the past half century or
so, there has been a steady decline in gastric cancer incidence and gastric
cancer deaths in men and women in the United States. Most of this
decrease has occurred in the intestinal type of gastric cancer. In addition,
the incidence of gastric cardia adenocarcinoma has actually gradually
increased.
The decrease in gastric cancer incidence may be attributed in part to the
adoption of diets high in vegetables and fruit. The widespread use of
refrigeration contributes to the decline in incidence by reducing the intake
of salt, which had been used as a food preservative, and decreasing the
contamination of food by carcinogenic compounds arising from the decay
of unrefrigerated meat products.
Salt and salted foods may cause damage to the gastric mucosa with
resultant inflammation associated with increase in DNA synthesis and cell
proliferation.
January 8, 2013 DR. RUBEL,SBMC 3

4. Epidemiology
Race
The rates of gastric cancer are higher in Asian and South American countries than
in the United States.
Japan, Chile, and Venezuela have developed a very rigorous early screening
program that detects patients with early stage disease (ie, low tumor burden). These
patients appear to do quite well.
In fact, in many Asian studies, patients with resected stage II and III disease tend
to have better outcomes than similarly staged patients treated in Western countries.
Some researchers suggest that this reflects a fundamental biologic difference in the
disease as it manifests in Western countries.
In the United States, Asian and Pacific Islander males and females have the
highest incidence of stomach cancer, followed by black, Hispanic, white, American
Indian, and Inuit populations.
January 8, 2013 DR. RUBEL,SBMC 4

5. Epidemiology-contd.
Sex
Gastric cancer affects slightly more men than women.
Age
Most patients are elderly at diagnosis. The median age for gastric cancer
in the United States is 70 years for males and 74 years for females. The
gastric cancers that occur in younger patients may represent a more
aggressive variant.
Mortality/Morbidity
The 5-year survival rate for curative surgical resection ranges from 30-
50% for patients with stage II disease and from 10-25% for patients with
stage III disease. Because these patients have a high likelihood of local
and systemic relapse, some physicians offer them adjuvant therapy. The
operative mortality rate for patients undergoing curative surgical
resection at major academic centers is less than 3%.
January 8, 2013 DR. RUBEL,SBMC 5

6. Surgical anatomy
The stomach begins at the gastroesophageal junction and ends at the duodenum. The stomach
has 3 parts. The uppermost part of the stomach is the cardia, and the largest and middle part is
called the body. The distal portion of the stomach, the pylorus, connects to the duodenum.
These anatomic zones have distinct histologic features. The cardia contains predominantly
mucin-secreting cells. The fundus (ie, body) contains mucoid cells, chief cells, and parietal cells,
while the pylorus is composed of mucus-producing cells and endocrine cells.
The stomach wall is made up of 5 layers. From the lumen out, the layers include the mucosa, the
submucosa, the muscularis layer, the subserosal layer, and the serosal layer.
The peritoneum of the greater sac covers the anterior surface of the stomach. A portion of the
lesser sac drapes posteriorly over the stomach. The gastroesophageal junction has limited or no
serosal covering.
The right portion of the anterior gastric surface is adjacent to the left lobe of the liver and the
anterior abdominal wall. The left portion of the stomach is adjacent to the spleen, the left adrenal
gland, the superior portion of the left kidney, the ventral portion of the pancreas, and the transverse
colon.
The site of the cancer is classified on the basis of its relationship to the long axis of the stomach.
Approximately 40% of cancers develop in the lower part, 40% in the middle part, and 15% in
the upper part, and 10% involve more than one part of the organ.
January 8, 2013 DR. RUBEL,SBMC 6

7. Causes
Several factors are implicated in the development of gastric cancer, including diet,
Helicobacter pylori infection, previous gastric surgery, pernicious anemia, adenomatous
polyps, chronic atrophic gastritis, prior radiation exposure or inherited syndromes.
Gastric cancer may often be multifactorial involving both inherited predisposition and
environmental factors.
Diet
A diet rich in pickled vegetables, salted fish, excessive dietary salt, and smoked meats
correlates with an increased incidence of gastric cancer.
A diet that includes fruits and vegetables rich in vitamin C may have a
protective effect.
Smoking
Smoking is associated with an increased incidence of stomach cancer in a dose-
dependent manner, both for number of cigarettes and duration of smoking.
Smoking increases the risk of cardiac and noncardiac forms of stomach
cancer. Cessation of smoking reduces the risk.
A meta-analysis of 40 studies estimated that the risk was increased by
approximately 1.5- to 1.6-fold and was higher in men.
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8. Helicobacter pylori infection
Chronic bacterial infection with H pylori is the strongest risk factor for stomach cancer.
H pylori may infect 50% of the world's population, but much less than 5% of infected
individuals develop cancer. It may be that only a particular strain of H pylori, one
which is capable of producing the greatest amount of inflammation, is especially
associated with the risk of malignancy. The full malignant transformation of affected
parts of the stomach may require that the human host have a particular genotype of
interleukin-Iβ to cause the increased inflammation and an increased suppression of
gastric acid secretion.
H pylori infection is associated with chronic atrophic gastritis, and patients with a
history of prolonged gastritis have a 6-fold increase in their risk of developing gastric
cancer. Interestingly, this association is particularly strong for tumors located in the
antrum, body, and fundus of the stomach but does not seem to hold for tumors
originating in the cardia.
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Causes-contd.

9. Previous gastric surgery
Previous surgery is implicated as a risk factor. The rationale is
that surgery alters the normal pH of the stomach which may in
turn lead to metaplastic and dysplastic changes in luminal cells.
Retrospective studies demonstrate that a small percentage of
patients who undergo gastric polyp removal have evidence of
invasive carcinoma within the polyp. This discovery has led some
researchers to conclude that polyps might represent
premalignant conditions.
Causes-contd.
January 8, 2013 DR. RUBEL,SBMC 9

10. Genetic factors
Some 10% of stomach cancer cases are familial in origin.
Genetic factors involved in gastric cancer remain poorly understood, though
specific mutations have been identified in a subset of gastric cancer patients. For
example, germ-line truncating mutations of the E-cadherin gene are detected in
50% of diffuse-type gastric cancers and families that harbor these mutations have
an autosomal dominant pattern of inheritance with a very high penetrance.
Other hereditary syndromes with a predisposition for stomach cancer include
hereditary nonpolyposis colorectal cancer, Li-Fraumeni syndrome, familial
adenomatous polyposis, and Peutz-Jeghers syndrome.
Ebstein-Barr virus: The Epstein-Barr virus may be associated with an unusual
form of stomach cancer (<1%), lympho-epitheliomalike carcinoma.
Pernicious anemia: Pernicious anemia associated with advanced atrophic
gastritis and intrinsic factor deficiency is a risk factor for gastric carcinoma.
January 8, 2013 DR. RUBEL,SBMC Causes-contd. 10

11. Gastric ulcers
Gastric cancer may develop in the remaining portion of the
stomach following a partial gastrectomy for gastric ulcer.
Benign gastric ulcers may themselves develop into
malignancy.
Obesity: Obesity increases the risk of gastric cardiac cancer.
Radiation exposure: Atomic bomb survivors exposed to radiation
have had an increased risk of stomach cancer. Other populations
exposed to radiation may also have an increased risk of stomach
cancer.
January 8, 2013 DR. RUBEL,SBMC Causes-contd.
11

12. Premalignant conditions;
H. pylori infection
Atrophic gastritis and pernicious anemia
Gastric polyps
Gastric ulcer
Hypergastrinemia
Blood group A
Previous gastric resection
Ménétrier’s disease
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13. Factors associated with increased risk of
developing stomach cancer
Nutritional
Low fat or protein consumption
Salted meat or fish
High nitrate consumption
High complex-carbohydrate consumption
Environmental
Poor food preparation (smoked, salted)
Lack of refrigeration
Poor drinking water (well water)
Smoking
Social
Low social class
Medical
Prior gastric surgery
Helicobacter pylori infection
Gastric atrophy and gastritis
Adenomatous polyps
Male gender
January 8, 2013 DR. RUBEL,SBMC 13

14. Correa mode of the pathogenesis of human gastric
adenocarcinoma
January 8, 2013 DR. RUBEL,SBMC 14

15. Histopathology
Adenocarcinoma 95%
Lymphomas 2%
Carcinoids 1%
Adenocathomas 1%
Squamous cell 1%
Adenocarcinoma is classified according to the most
unfavorable microscopic element present: tubular,
papillary, mucinous, signet-ring cells.
Also identified by gross appearance: ulcerative,
polypoid, scirrous, superficial spreading,
multicentric, or Barrett ectopic.
Variety of other schemes: Borrmann, Lauren
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16. Borrmann Classification
5 categories
Type I: polypoid or fungating
Type II: ulcerating lesions with elevated borders
Type III: ulceration with invasion of wall
Type IV: diffuse infiltration
Type V: cannot be classified
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17. Borrmann types
Borrmann I
Borrmann II
Borrmann III
Borrmann IV
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18. Lauren system
The intestinal type
 Expansive epidemic type gastric cancer is associated
with atrophic gastritis, retained glandular structure,
little invasiveness, sharp margins. It would be a
Borrmann I or II, carries better prognosis, shows no
family history
The diffuse type
 Infiltrative, endemic, is poorly differentiated, with
dangerously deceptive margins, invades large areas
of stomach. Younger patients, genetic factors, blood
groups, and family history.
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19. Lauren system
The most useful classification of gastric cancer is the Lauren Classification System. The
Lauren system classifies gastric cancer pathology as either
Type I (intestinal)
Type II (diffuse).
Intestinal type - expansive, epidemic, gastric cancer is associated with chronic atrophic
gastritis, retained glandular structure, little invasiveness, with sharp margin, associated
with most environmental risk factors, carries a better prognosis, and shows no familial
history.
Diffuse type - infiltrative, endemic cancer, consists of scattered cell clusters with poor
differentiation and dangerously deceptive margins. The endemic-type tumor invades
large areas of the stomach. This type of tumor is also not recognizably influenced by
environment or diet, is more virulent in women, and occurs more often in relatively
young patients. This pathologic entity is associated with genetic factors (such as E-
cadherin), blood groups A, and a family history of gastric cancer.
Intestinal Diffuse
Environmental Familial
Gastric atrophy, intestinal metaplasia Blood type A
Men > women Women > men
Increasing incidence with age Younger age group
Microscopic Microscopic
Gland formation Poorly differentiated signet ring cells
Hematogenous spread Transmural/lymphatic spread
Microsatellite instability Decreased E-cadherin
APC gene mutations APC gene mutations
p53, p16 inactivation p53, p16 inactivation
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20. According to the clinical presentation &
treatment planning gastric cancer are grossly
classified as follows:
A. Early Gastric Cancer (EGC)
B. Advanced Gastric Cancer (AGC)
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21. .
Early Gastric Cancer
The term 'early gastric cancer' is
used to describe tumours confined
to the gastric mucosa and
submucosa, irrespective of nodal
status, and was elaborated in 1962
by the Japanese Society of
Gastroenterological Endoscopy
Type I Exophytic lesion extending into the
gastric lumen
Type II Superficial variant
II A Elevated lesions with a height
no more than the thickness of the adjacent
mucosa
II B Flat lesions
II C Depressed lesions with an
eroded but not deeply ulcerated
appearance
Type III Excavated lesions that may
extend into the muscularis propria without
invasion of this layer by actual cancer cells
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22. Advanced gastric cancer:
 The vast majority of gastric cancer are of advanced which
deeply penetrate the stomach wall, invade the adjacent
structures with lymphatic & haematogenous metastasis.
 Advanced gastric cancer classified according to the
Bormann's morphologic description as -
Borrmann I: Fungating
Borrmann II: Carcimatous ulcer without
infiltrating surrounding mucosa
Borrmann III: Carcimatous ulcer with infiltration
of surrounding mucosa
Borrmann IV: Diffuse infiltrating carcinoma
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23. Advanced Gastric Cancer - Morphological
Types;
PPolypoidoid Borrmann I
Ulcerating
Borrmann II
Ulcerating/ Borrmann III
infiltrating
Diffuse
infiltrating Borrmann IV
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24. Borrmann's morphologic
description
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25. Spread
Pathophysiology;
Understanding the vascular supply of the stomach allows understanding of
the routes of hematogenous spread. The vascular supply of the stomach is
derived from the celiac artery. The left gastric artery, a branch of the celiac
artery, supplies the upper right portion of the stomach. The common hepatic
artery branches into the right gastric artery, which supplies the lower portion
of the stomach, and the right gastroepiploic branch, which supplies the lower
portion of the greater curvature.
Understanding the lymphatic drainage can clarify the areas at risk for nodal
involvement by cancer. The lymphatic drainage of the stomach is complex.
Primary lymphatic drainage is along the celiac axis. Minor drainage occurs
along the splenic hilum, suprapancreatic nodal groups, porta hepatis, and
gastroduodenal areas.
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26. Lymphatic drainage
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27. Lymphatic drainage
January 8, 2013 DR. RUBEL,SBMC 27

28. Gastric Lymphatics
Numbering of the gastric and upper
abdominal node stations
Station no. Anatomical location
1, 2 Adjacent to the cardia (perigastric)
3, 4 Adjacent to lesser and greatercurve
5 Suprapyloric (right gastric artery)
6 Infrapyloric
7 Left gastric artery
8 Common hepatic artery
9 Coeliac artery
10 Hilum of the spleen
11 Splenic artery
12 Hepaticoduodenal ligament
13 Behind pancreatic head
14 At the root of the mesentery
(superior mesenteric artery)
15 Middle colic artery
16 Para-aortic

29. Gastric Lymphatics
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30. Spread patterns
Cancer of the stomach can spread directly, via lymphatics, or hematogenously and
transperitonialy.
Direct extension into the omenta, pancreas, diaphragm, transverse colon
or mesocolon, and duodenum is common.
If the lesion extends beyond the gastric wall to a free peritoneal (ie,
serosal) surface, then peritoneal involvement is frequent.
The visible gross lesion frequently underestimates the true extent of the
disease.
The abundant lymphatic channels within the submucosal and subserosal
layers of the gastric wall allow for easy microscopic spread.
The submucosal plexus is prominent in the esophagus and the subserosal
plexus is prominent in the duodenum, allowing proximal and distal spread.
Lymphatic drainage is through numerous pathways and can involve
multiple nodal groups (eg, gastric, gastroepiploic, celiac, porta hepatic,
splenic, suprapancreatic, pancreaticoduodenal, paraesophageal, and
paraaortic lymph nodes).
The cancer also spreads hematogenously, and liver metastases are
common.
The cancer also spreads transperitonialy to other abdominal organs as
omentum peritoneum, and especially to ovary as Krukenberg’s tumor.
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31. Clinical
History
In the United States, about 25% of stomach cancer cases present with localized
disease, 31% present with regional disease, and 32% present with distant
metastatic disease; the remainder of cases surveyed were listed as unstaged.
Early disease has no associated symptoms; however, some patients with
incidental complaints are diagnosed with early gastric cancer. Most symptoms of
gastric cancer reflect advanced disease. Patients may complain of indigestion,
nausea or vomiting, dysphagia, postprandial fullness, loss of appetite, melena,
hematemesis, and weight loss.
Late complications include pathologic peritoneal and pleural effusions;
obstruction of the gastric outlet, gastroesophageal junction, or small bowel;
bleeding in the stomach from esophageal varices or at the anastomosis after
surgery; intrahepatic jaundice caused by hepatomegaly; extrahepatic jaundice;
and inanition resulting from starvation or cachexia of tumor origin.
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32. Clinical-contds.
Physical
All physical signs are late events, and almost invariably the signs develop too late
for curative procedures.
Signs may include a palpable enlarged stomach with succussion splash;
hepatomegaly; periumbilical metastasis (Sister Mary Joseph nodule); enlarged lymph
nodes such as: Virchow’s nodes (ie, left supraclavicular), Irish node (anterior
axillary); and Blumer shelf (ie, shelflike tumor of the anterior rectal wall).
Some patients experience weight loss and others may present with melena or
pallor from anemia.
Paraneoplastic syndromes such as dermatomyositis, acanthosis nigricans, and
circinate erythemas are poor prognostic features.
Other associated abnormalities also include peripheral thrombophlebitis and
microangiopathic hemolytic anemia.
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33. Clinical presentation:
There are five group of clinical presentation, which are as follows -
New dyspepsia after 40 - persistent indigestion in a patient who has
never had previous stomach trouble. It was one of the manifestation of
our presented case.
Obstructive type - carcinoma of the pyloroantrum may present with
abdominal fullness & vomiting which was the predominant manifestation
of our presented case. Carcinoma of the cardia may present with
dysphagia & regurgitation
Abdominal lump - epigastric lump is the presenting feature of about
30% of cases
Insidious - sometimes patient may present with only tiredness, marked
anorexia, asthenia & evidence of anaemia.
Silent - carcinoma of the gastric body may present with metastatic
manifestations like jaundice, enlarged left supraclavicular lymph
nodes(Virchow’s gland),ascites, rectal shelf of Blummer(Metastatic nodule on
the rectal wall),Sister Joseph’s nodules(Metastatic nodule on the
umbilicus),Krukenberg’s tumors(Metastasis on ovary).
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34. Lab Studies
The goal of obtaining laboratory studies is to assist in
determining optimal therapy.
A complete blood cell count can identify anemia,
which may be caused by bleeding, liver dysfunction,
or poor nutrition. Approximately 30% of patients
have anemia.
Electrolyte panels and liver function tests also
are essential to better characterize the patient's
clinical state.
Carcinoembryonic antigen (CEA) is increased in
45-50% of cases.
Cancer antigen (CA) 19-9 is elevated in about
20%of cases.
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35. Imaging Studies
Esophagogastroduodenoscopy has a diagnostic accuracy of
95%. This relatively safe and simple procedure provides a permanent
color photographic record of the lesion.
This procedure is also the primary method for obtaining a tissue
diagnosis of suspected lesions. Biopsy of any ulcerated lesion
should require at least 6 biopsies taken from around the lesion
because of variable malignant transformation.
In selected cases, endoscopic ultrasound may be helpful in
assessing depth of penetration of the tumor or involvement of
adjacent structures.
Double-contrast upper gastrointestinal series and barium
swallows may be helpful in delineating the extent of disease when
obstructive symptoms are present or when bulky proximal tumors
prevent passage of the endoscope to examine the stomach distal to an
obstruction (more common with gastroesophageal [GE]-junction
tumors). These studies are only 75% accurate and should for the most
part be used only when upper GI endoscopy is not feasible.
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36. Imaging Studies-contd.
Chest radiograph is done to evaluate for metastatic lesions.
CT scan or MRI of the chest, abdomen, and pelvis assess the
local disease process as well as evaluate potential areas of spread
(ie, enlarged lymph nodes, possible liver metastases).
Endoscopic ultrasound allows for a more precise preoperative
assessment of the tumor stage. Endoscopic sonography is becoming
increasingly useful as a staging tool when the CT scan fails to find
evidence of T3, T4, or metastatic disease.
Institutions that favor neoadjuvant chemoradiotherapy for patients
with locally advanced disease rely on endoscopic ultrasound data to
improve patient stratification.
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37. Histologic Findings
Adenocarcinoma of the stomach constitutes 90-95% of all
gastric malignancies. The second most common gastric
malignancies are lymphomas. Gastrointestinal stromal tumors
formerly classified as either leiomyomas or leiomyosarcomas
account for 2% of gastric neoplasms, Carcinoids (1%),
adenoacanthomas (1%), and squamous cell carcinomas (1%)
Adenocarcinoma of the stomach is subclassified according to
histologic description as follows: tubular, papillary, mucinous, or
signet-ring cells, and undifferentiated lesions.
Pathology specimens are also classified by gross appearance. In
general, researchers consider gastric cancers ulcerative, polypoid,
scirrhous (ie, diffuse linitis plastica), superficial spreading,
multicentric, or Barrett ectopic adenocarcinoma.
The Lauren system classifies gastric cancer pathology as either
Type I (intestinal) or Type II (diffuse). An appealing feature of
classifying patients according to the Lauren system is that the
descriptive pathologic entities have clinically relevant differences.
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38. TNM Classification of
Carcinoma of the Stomach
Primary tumor (T)
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
Tis Carcinoma in situ: intraepithial tumor without
invasion of the lamina propria
T1 Tumor invades lamina propria or submucosa
T2 Tumor invades muscularis propria or subserosa
T2a Tumor invades mucularis propria
T2b Tumor invades subserosa
T3 Tumor penetrates serosa (visceral peritoneum)
without invasion of adjacent structures
T4 Tumor invades adjacent structures
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39. TNM Classification of Carcinoma of the Stomach-
contd.
Regional lymph nodes (N)
NX Regional lymph node(s) cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis in 1 to 6 regional lymph nodes(perigastric groups)
N2 Metastasis in 7 to 15 regional lymph nodes(coeliac groups)
N3 Metastasis in more than 15 regional lymph nodes(para-aortic groups)
Distant metastasis (M)
MX Distant metastasis
cannot be assessed
M0 No distant metastasis
M1 Distant metastasis
Lymph node station numbers as defined by the
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Japanese Gastric Cancer Association

40. Surgical Treatment
Surgical resection provides the only hope for curing gastric cancer.
Even then, some patients show criteria of inoperability at the time of
presentation. These include the presence of Virchow’s node, obvious
liver metastasis, rectal shelf, and ascites.
The type of gastric resection needed depends on location of the tumor.
In all cases, proximal and distal surgical margins should be clear of
tumor for at least 4 to 6 cm. When the resection required is distal
gastrectomy, the following surgical strategies should also be employed:
1. Resection of the duodenal bulb and Bilroth II reconstruction.
2. Division of left and right gastric arteries at their origin, and
3. Removal of the greater omentum.
It is always useful to do preoperative bowel preparation in the event that
the transverse colon has to be resected en bloc.
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Surgical Treatment-contd.

41. Surgical Treatment-contd.
The main controversy relates to the extent of lymph
node dissection. Types of resective surgery have been
classified based on this criterion as follows:
1. R1: complete removal of perigastric lymph
nodes;
2. R2: resection of perigastric nodes and those
along the left gastric, splenic, and right hepatic
arteries;
3. R3: R2 with dissection of celiac axis nodes;
4. R4: R3 with dissection of paraaortic nodes.
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42. A-Subtotal gastrectomy with a Billroth II anastomosis.
B-Total gastrectomy with a Roux-en-Y anastomosis.
A
B
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43. Surgical Treatment
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44. Endoscopic Resection
The Japanese have demonstrated that some patients with early
gastric cancer can be adequately treated by an endoscopic
mucosal resection.
Small tumors (<3 cm) confined to the mucosa have an
extremely low chance of lymph node metastasis (3 percent) which
approaches the operative mortality rate for
gastrectomy.
If the resected specimen demonstrates no ulceration, no
lymphatic invasion, and size less than 3 cm, the risk of lymph
node metastases is less than 1 percent.
Thus some patients with early gastric cancer might be better
treated with the endoscopic technique. Currently this should be
limited to patients with tumors less than 2 cm, which on EUS are
node-negative and confined to
the mucosa.
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45. PALLIATIVE TREATMENT
Because 20% to 30% of gastric cancer patients present with stage IV
disease, clinicians must be familiar with different methods of palliative
treatment. The goal of palliative treatment is the relief of symptoms with
minimal morbidity.
Surgical palliation of advanced gastric cancer may include resection or
bypass alone or in conjunction with percutaneous, endoscopic, or
radiotherapeutic techniques.
Complete staging is necessary to determine the appropriate method of
palliation for individual patients.
In the presence of peritoneal disease, hepatic metastases, diffuse nodal
metastases, or ascites, palliation of bleeding or proximal gastric
obstruction would preferably be obtained nonoperatively.
Nonoperative therapies include laser recanalization and endoscopic
dilation, with or without stent placement. Patients who undergo stent
placement for gastric outlet obstruction are frequently able to tolerate
solid foods and may not require additional interventions.
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46. Adjuvant Therapy
Adjuvant treatment with chemotherapy (5 FU and leucovorin) and
radiation (4500 cGy) has demonstrated a survival benefit in resected
patients with stageII and III adenocarcinoma of the stomach.
There is no indication for the routine use of radiation alone in the
adjuvant setting, but in certain patients it can be very effective
palliation for bleeding or pain.
In patients with gross unresectable, metastatic, or recurrent disease,
palliative chemotherapy has not been demonstrated to conclusively
prolong survival, but an occasional patient has a dramatic response.
These patients should be considered for clinical trials.
Agents that have shown activity against gastric cancer include 5 FU,
cisplatin, adriamycin, and methotrexate.
Neoadjuvant treatment of gastric adenocarcinoma is being evaluated.
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47. Five-Year Survival Rate of Patients
with Stomach Cancer
Tumor stage % Survival
R1 resection R2 resection
IA 88 91
IB 56 85
II 39 58
IIIA 7 30
IIIB 0 12
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48. OUTCOMES
Survival rates for all patients with gastric carcinoma
stratified by combined American Joint Committee on Cancer
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49. OUTCOMES-contd.
Survival rates for gastric cancer patients undergoing gastrectomy
as stratified by combined American Joint Committee on Cancer
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50. Recurrence
Recurrence rates after gastrectomy remain high, ranging from
40% to 80%, depending on the series. Most recurrences occur
within the first 3 years.
The locoregional failure rate ranges from 38% to 45%, whereas
peritoneal dissemination as a component of failure occurs in 54%
of patients in several series.
Isolated distant metastases are uncommon, because most
patients with distant failure also have locoregional recurrence as
well.
The most common sites of locoregional recurrence are the
gastric remnant at the anastomosis and in the gastric bed and
the regional nodes. Hematogenous spread occurs to the liver,
lung, and bone.
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51. SURVEILLANCE
All patients should be followed up systematically. Because most
recurrences occur within the first 3 years, surveillance
examinations are more frequent in the first several years.
Follow-up should include a complete history and physical
examination every 4 months for 1 year, then every 6 months for
2 years and then annually thereafter.
Laboratory examinations including complete blood counts and
liver function tests should be obtained as clinically indicated.
Many clinicians obtain chest radiographs as well as CT scans of
the abdomen and pelvis routinely, wheresas others obtain
studies only when clinically suspicious of a recurrence. Yearly
endoscopy should be considered in patients who have
undergone a subtotal gastrectomy.
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52. Screening for Gastric Cancer
In Japan it has clearly been shown that patients participating in
gastric cancer screening programs have a significantly decreased
risk of dying from gastric cancer. Thus screening is effective in a
high risk population.
Certainly screening the general population in a low-risk country
does not make sense, but patients clearly at risk for gastric cancer
should probably have periodic endoscopy and biopsy. This includes
patients with FAP, HNPCC, gastric adenomas, Menetrier disease,
intestinal metaplasia, dysplasia, and remote gastrectomy or
gastrojejunostomy.
January 8, 2013 DR. RUBEL,SBMC 52

53. Summary Aetiology
Definition The following are predisposing
Malignant lesion of the stomach factors.
epithelium. • Diet (smoked fish, pickled
vegetables, benzpyrene,
Key points nitrosamines).
• The majority of tumours are • Atrophic gastritis.
unresectable at presentation. • Pernicious anaemia.
• Tumours considered candidates for • Previous partial gastrectomy.
resection should be staged with • Familial hypogammaglobulinaemia.
CT and laparoscopy to reduce the risk of • Gastric adenomatous polyps.
an ‘open and shut’ laparotomy. • Blood group A.
• Most tumours are poorly responsive to
chemotherapy. Pathology
• Histology: adenocarcinoma.
Epidemiology • Advanced gastric cancer
Male/female 2 : 1, peak incidence 50+ (penetrated muscularis propria) may
years. Incidence has be polypoid, ulcerating or infiltrating
decreased in Western world over last 50 (i.e. linitus plastica).
years. Still common in • Early gastric cancer (confined to
Japan, Chile and Scandinavia. mucosa or submucosa).
January 8, 2013 DR. RUBEL,SBMC 53

54. Spread
lymphatic (e.g. Virchow’s node); haematogenous to Essential management
liver, lung, brain; transcoelomic to ovary • Palliation (metastatic disease or
(Krukenberg tumour). gross distal nodal disease at
presentation):
Clinical features gastrectomy: local symptoms, e.g.
• History of recent dyspepsia (epigastric discomfort, bleeding;
postprandial gastroenterostomy: malignant pyloric
fullness, loss of appetite). obstruction;
• Anaemia. intubation: obstructing lesions at the
• Dysphagia. cardia.
• Vomiting. • Curative treatment (resectable
• Weight loss. primary and local nodes).
• The presence of physical signs usually indicates • Surgical excision with clear margins
advanced and locoregional lymph node
(incurable) disease. clearance (D2 gastrectomy).
• Other treatment: combination
Investigations chemotherapy with etoposide,
• FBC. adriamycin and cisplatin may induce
• U+E. regression.
• LFTs. Prognosis
• OGD (see the lesion and obtain biopsy to Following ‘curative’ resection, 5-year
distinguish from survival rates are approximately 20%,
benign gastric ulcer). but overall 5-year survival (palliation
• Barium meal (space-occupying lesion/ulcer with and resection) is only 5%.
rolled edge).
Best for patients unable to tolerate OGD.
• CT scan (helical): stages disease locally and
systemically.
• Laparoscopy: used to exclude undiagnosed
peritoneal or8, 2013
January liver secondaries prior to consideration
DR. RUBEL,SBMC 54

55. January 8, 2013 DR. RUBEL,SBMC 55