A CLINICOPATHOLOGICAL STUDY OF

GASTRIC CARCINOMA

By

Dr. ROMMEL. S, M.B.B.S

Dissertation Submitted to the
Rajiv Gandhi University of Health Sciences, Karnataka
In partial fulfillment
of the requirements for the degree of

MASTER OF SURGERY
in

GENERAL SURGERY
Under the guidance of

Prof. B. JAGADISH M.S.

Professor and Unit Chief
Department of Surgery

MYSORE MEDICAL COLLEGE AND RESEARCH INSTITUTE,

MYSORE
APRIL 2011
i

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES

DECLARATION BY THE CANDIDATE

I hereby declare that this dissertation entitled A CLINICOPATHOLOGICAL

STUDY OF GASTRIC CARCINOMA is a bonafide and genuine research work
carried out by me under the guidance of my Guide Prof. B. JAGADISH,

MS.

Department of General Surgery, and with Prof. Mudassir Azeez Khan, Department of
Community Medicine and Prof. Nataraju G., Department of Pathology Mysore
Medical College and Research Institute, Mysore as Co-Guides

Date:
Place: Mysore

ii

CERTIFICATE BY THE GUIDE

This is to certify that the dissertation entitled A CLINICOPATHOLOGICAL

STUDY OF GASTRIC CARCINOMA is a bonafide research work done by
Dr. Rommel .S. in partial fulfillment of the requirement for the degree of Master of
Surgery in General Surgery.

Date:
Place: Mysore

iii

CERTIFICATE BY THE CO-GUIDES

This is to certify that the dissertation entitled A CLINICOPATHOLOGICAL

STUDY OF GASTRIC CARCINOMA is a bonafide research work done by
Dr. Rommel .S. in partial fulfillment of the requirement for the degree of Master of
Surgery, General Surgery.

iv

ENDORSEMENT BY THE HEAD OF THE DEPARTMENT AND

PRINCIPAL

This is to certify that the dissertation entitled A CLINICOPATHOLOGICAL

STUDY OF GASTRIC CARCINOMA is a bonafide research work done by Dr.
ROMMEL. S. under the guidance of Prof. B. JAGADISH, Professor of Surgery,
Department of General Surgery, at K.R. Hospital attached to Mysore Medical College
and Research Institute, Mysore.

COPYRIGHT
Declaration of the candidate

I hereby declare that The Rajiv Gandhi University of Health

Sciences, Karnataka shall have the rights to preserve, use and
disseminate this dissertation/ thesis in print or electronic format
for academic/ research purpose.

Date:
Place: Mysore

Dr. ROMMEL. S
Post Graduate in General
Surgery
Mysore Medical College
and Research Institute,
Mysore

Rajiv Gandhi University of Health Sciences, Karnataka

vi

ACKNOWLEDGEMENT
It gives me great pleasure in preparing this dissertation and I take this opportunity to
thank everyone who has made this possible. It is most appropriate that I begin by
expressing my gratitude to the Almighty for his Blessings.
I express my deep sense of gratitude and indebtedness to my most respected guide and
treasured teacher Prof. B. Jagadish. M.S., Professor and Unit Chief, Department of
Surgery, Mysore Medical College and Research Institute, Mysore whose wisdom and
appropriate blend of science and art in the practice of surgery has been and will
always be a constant source of encouragement.
I express my deep sense of gratitude to my Co-guides, Prof. Mudassir Azeez Khan,
Head of thye Department of Community Medicine and Prof. Nataraju G., Department
of Pathology for their support and guidance throughout this study.
I express my sincere thanks to Dr. AVADHANI GEETA. K., Professor and HOD of
Surgery, MMC&RI Mysore for her valuable advice and support.
I am also thankful to Assistant Professor Dr. Balasubrahmanya and Senior Resident
Dr. B.G. Ponnappa

for their constant support, encouragement and valuable

suggestions.
I thank all the staff of the Department of General Surgery for all the help rendered.
I owe a lot to my post graduate colleagues and interns for their encouragement and
enthusiastic co- operation.
I always remember my family especially my brother for his support and
encouragement.
vii

I would like to thank Dr. Swati Kaktikar without whose help this would not have been
possible.
Lastly I would like to thank all the patients and their attenders for their co-operation.

Date :
Dr.ROMMEL. S

Place : Mysore

viii

LIST OF ABBREVIATIONS USED

(in alphabetical order)

M- Moderate

A-Ascites

MA Minimal Ascites

B- Body

MRD- Medical Renal Disease

C- Cardia

O- Operable

D-Diffuse

P- Poor

DC- Decreased capacity

PA- Pyloric Antrum

DS- Dilated Stomach

PALN- Paraaortic Lymph nodes

EL- Emergency Laparotomy

PE- Pleural effusion

EP- Enlarged Prostate

Per- Perforation

F-Fundus

Po- Polypoidal

FJ- Feeding Jejunostomy

PO- Pyloric Obstruction

G- Growth

PG- Partial Gastrectomy

GEJ- Gastro-oesophageal junction

PGJ- Palliative GJ

GC- Greater curvature

PGLN- Perigastric Lymph Nodes

HPR- Histopathology report

PHLN- Porta Hepatis Lymph Nodes

I- Infiltrative

PR- Per rectal examination

IO- Inoperable

S-Splenomegaly

JJ- Jejunojejunostomy

SWT- Stomach wall thickening

LC- Lesser curvature

U-Ulcerative

LS- Liver secondaries

UGI- Upper gastrointestinal

ix

ABSTRACT
Background

Cancer is the second most common cause of cancer related deaths worldwide. Major
changes have been noted in the site of gastric cancer occurrence. The west has noted a
paradigm shift with a steady increase in cancers of the proximal stomach and a
decline in cancers of the distal stomach. Gastric cancer is well known to be associated
with risk factors
Objectives
This study was undertaken at K.R. Hospital, Mysore attached to Mysore Medical
College and Research Centre to study the trends regarding prevalence, clinical
features, association of risk factors, site of occurrence and histopathology.
Methods
All patients with histological confirmation of gastric carcinoma attending
K.R.Hospital from January 2009 to July 2010 were studied and details regarding the
clinical presentation, sub site, pathological features and treatment were collected.
Results
Thirty two patients with histological confirmation of carcinoma stomach were
studied. Gastric carcinoma was seen in the older age group with male preponderance.
The association of risk factors was studied. Majority of the patients presented in the
advanced stage and distal tumours were the predominant subtype.
Interpretation and Conclusion
Gastric cancer is a common malignancy in this part and is commonly seen in the older
age group predominantly in males. Patients usually present in the advanced stage,
x

however with the increasing use of upper gastrointestinal endoscopy early gastric
cancers are also being detected.
The association of risk factors is well known and consistent and hints at the
primordial prevention of the disease.
Unlike in the west where there has been a shift in the site of the tumour, distal
tumours continue to be the major subtype in this study.
A multidisciplinary approach combining population screening with molecular
biological techniques that are being developed is required to detect the cancer early
and improve prognosis.

xi

TABLE OF CONTENTS
SI
No.

Contents

Page
number

Introduction

Objectives

Review of Literature

Methodology

56

Results

58

Discussion

79

Conclusion

85

Summary

87

Bibliography

88

10

Annexures

94

xii

LIST OF TABLES

Sl. No

Tables

Pages

Lauren Classification System

12

Genetic Abnormalities in Gastric Cancer

17

TNM staging of gastric cancer

34

Stage grouping gastric carcinoma

34

Japanese Gastric Cancer Association Staging System for

Gastric Cancer

36

6
7
8
9
10
11
12
13
14
15
16
17
18

Sex distribution among carcinoma stomach patients

Age distribution among carcinoma stomach patients
Income group among carcinoma stomach patients

38
60
61

Comparison of risk factors between males and females

62

Blood group distribution in carcinoma stomach patients

64

Symptom analysis in patients of carcinoma stomach

66

Analysis of signs in gastric cancer patients

68

Sub site specific trends in carcinoma stomach

70

Comparison of the macroscopic type in both sexes

71

Comparision of symptoms with the site of the tumour

72

Comparision of symptoms with macroscopic appearance

73

Analysis of the site of tumour with signs

74

Comparison of macroscopy with clinical signs

75

xiii

19
20
21
22
23
24
25
26
27
28

Comparison of histopathology

76

Comparision of histology with the site of the tumour

77

Sex distribution among carcinoma stomach patients

80

Age distribution among carcinoma stomach patients

80

Socioeconomic groups among gastric cancer patients

81

Blood group distribution in carcinoma stomach patients

81

Comparison of risk factors between males and females

82

Symptom analysis in patients of carcinoma stomach

83

Sub site specific trends in carcinoma stomach

83

Comparison of histology according to Broders classification

84

xiv

LIST OF FIGURES
Sl.No

Figures

Pages

Borrmann classification of gastric carcinoma

Photomicrographs of gastric adenocarcinoma.

12

Role of Helicobacter pylori

17

T Stage defined by depth of penetration into gastric wall

34

Lymph node station numbers as defined by Japanese Cancer

Association

37

Japanese classification system for early gastric cancer

41

Endoscopic photograph showing ulceroproliferative growth in

antrum

98

Endoscopic photograph showing early gastric cancer

98

Photograph showing gastric cancer invading the posterior wall and

perforating it

99

10

Photograph showing palliative anterior gastrojejunostomy

99

11

Photograph showing partial gastrectomy specimen

100

12

Photograph showing opened partial gastrectomy specimen

100

xv

INTRODUCTION

INTRODUCTION
Adenocarcinoma of the stomach was the leading cause of cancer-related
death worldwide through most of the 20th century. It now ranks second only to
lung cancer, and an estimated 875,000 new cases are diagnosed annually
worldwide. In many parts of the world, however, the incidence of gastric cancer
has gradually decreased, principally because of changes in diet, food preparation,
and other environmental factors. The declining incidence has been dramatic in the
United States, where this disease ranks seventh as a cause of cancer-related deaths.
Stomach cancer incidence rates are much lower in India than elsewhere, but the
stomach remains one of the 10 leading sites of cancer in both sexes in most of the
metropolitan registries. Cancer rates in India are rising with increasing migration
of rural population to the cities, increase in life expectancy and changes in
lifestyles.

Change of diet is among the factors that may be responsible for the
changing disease rates. Diet in India encompasses diversity unknown to most other
countries, with many dietary patterns emanating from cultural and religious
teachings that have existed for thousands of years. Very little is known, however,
about the role of the Indian diet in causation of cancer or its role, if any, in
prevention of cancer, although more attention is being focused on certain aspects
of the Indian diet, such as vegetarianism, spices, and food additives.

The prognosis for this disease remains poor except in a few countries. The
explanations for these poor results are multifactorial. The lack of defined risk
factors and specific symptoms and the relatively low incidence have contributed to
the late stage at diagnosis seen in most Western countries. In Japan, where gastric
cancer is endemic, more patients are diagnosed at an early stage, which is reflected
by higher overall survival rates.

Although the incidence of gastric cancer has decreased dramatically over

the past century, the decline has been limited to cancers below the esophagogastric
junction. The number of newly diagnosed cases of proximal gastric and
esophagogastric junction adenocarcinomas has increased markedly since the mid1980s. These tumors are thought to be biologically more aggressive than distal
tumors and more complex to treat.

The only proven, potentially curative treatment for gastric cancer is

surgical resection of all gross and microscopic disease. Even after what is felt to
be a curative gastrectomy, disease recurs in both regional and/or distant sites in the
majority of patients. Efforts to improve these poor results have focused on
developing effective pre- and postoperative systemic and regional adjuvant
therapies.

AIMS AND OBJECTIVES OF THE STUDY

1. To study the prevalence of carcinoma stomach as occurring in K.R.Hospital ,

Mysore.
2. To study the clinical presentation including the anatomic site of occurrence and
Histological type
3. To study the association of risk factors
4. To study the surgical modalities of treatment

REVIEW OF LITERATURE
The stomach is a remarkable organ with important digestive, nutritional,
and endocrine functions. The stomach stores and facilitates the digestion and
absorption of ingested food, and it helps regulate appetite1. Wallace P. Ritchie, Jr.
called the stomach an elegant organ, once thought to be the seat of the soul,
always handy to bring to the dinner table, and a recognized source of ecstasy and
grief2. Approximately 90% of all tumours of the stomach are malignant, the vast
majority of which are adenocarcinoma.3

EPIDEMIOLOGY

Worldwide, gastric cancer remains the second or third most common

malignancy (nearly 900,000 new cases annually) and the second most common
cause of death (approximately 650,000 deaths).3, 4 The incidence of gastric cancer
has significant geographic variation, with the highest incidence (75 to 100 per
100,000 men) occurring in Japan, Korea and parts of South America and Eastern
Europe and the lowest incidence(as low as 5 per 100,000 men) occurring in the
United States and Western Europe.3,5

In India, the stomach was estimated to be the fifth leading site in males and
the seventh in females in 1991 with age-standardized rates (ASRs) of 5.0 and 2.8
per 100,000 in males and females, respectively.

With the establishment of the National Cancer Registry Programme, cancer

incidence data are available for 5 metropolitan areas and 1 rural area in India since
1982. From 1988 through 1992, the stomach was the leading site of cancer in
males in Chennai (ASR = 15.9 per 100,000) and Bangalore (ASR = 10.3), fifth in
Mumbai (ASR = 7.7) and fourth in Trivandrum (ASR = 6.8); among females, it
was the fourth leading site in Chennai (ASR = 7.0), fifth in Bangalore (ASR = 5.1)
and sixth in both Mumbai (ASR = 3.8) and Trivandrum (ASR = 2.5).6

In contrast with the general decline in incidence, an increase has been

observed for cardia lesions in many regions. Comparatively high rates are evident
for the United Kingdom/Ireland, Northern Europe, Australia and New Zealand,
China, and North America. The increase in incidence of cardia lesions has been
associated with parallel increases for adenocarcinomas of the lower esophagus,
where hyperacidity, reflux esophagitis, Barretts esophagus, and obesity have been
proposed as likely risk factors. 7 In a study conducted in Tamil Nadu, the sites of
gastric cancer in order of frequency were antrum (67.3%) followed by
body(23.3%), proximal stomach(5.6%) and OGJ(3.8%) .8 A recent study from the
southern state of Kerala showed that carcinoma of the distal stomach has remained
predominant although a trend towards a proximal shift has been noticed. 9

PATHOLOGY AND TUMOR BIOLOGY

Approximately

95%

of

all

malignant

gastric

neoplasms

are

adenocarcinomas, and in general, the term gastric cancer refers to adenocarcinoma

of the stomach. Other malignant tumors are very rare and include squamous cell
carcinoma, adenoacanthoma, carcinoid tumors, and leiomyosarcoma. Although no
normal lymphoid tissue is found in the gastric mucosa, the stomach is the most
common site for lymphomas of the gastrointestinal tract. 10

Morphologic features and classification

In 1965, Lauren described two histologic types of gastric adenocarcinoma,

intestinal and diffuse, which provided a model to understand better the etiology
and epidemiology of the disease.

Several pathologic classifications have been proposed based on the

morphologic features of gastric tumors.

The Borrmann classification divides gastric cancer into five types depending on
macroscopic appearance.

Type I represents polypoid or fungating cancers

Type II encompasses ulcerating lesions surrounded by elevated borders
Type

III

represents

ulcerated

lesions

infiltrating

Type IV are diffusely infiltrating tumors

Type V are unclassifiable cancers10,11

Fig. 1 Borrmann classification of gastric carcinoma

the

gastric

wall

Gross Morphology

There is wide variation in the gross appearance of carcinoma of stomach.

Many intermediate stages exist between the two extremes represented by the
fungating tumour growing mainly into the lumen and the flat, ulcerated and deeply
invasive tumour growing through the wall of the stomach.

Carcinomas located in the fundic area are more likely to have invaded the
submucosa and beyond at the time of surgery than those located in the pyloric
area.

Depending upon the relative amounts of mucin secreted and desmoplastic

reaction elicited, the tumour may have a fleshy, fibrous or gelatinous gross
appearance. In terms of location, any area of the stomach can be affected: anterior
and posterior wall, lesser curvature, and greater curvature (in that order of
frequency). Multiple tumours are found in approximately 6% of cases.

The non neoplastic mucosa adjacent to the carcinoma is often thickened; a

feature that may result in false negative endoscopic biopsies and that has been
attributed to production of epidermal growth factor by the tumour.

Microscopy

Nearly all gastric carcinomas are of the adenocarcinoma type and

composed of one or more of the following four major cell types- foveolar,
mucopeptic, intestinal columnar and goblet cell.

As, described by Lauren, two major categories exist, which have been designated
intestinal (53%) and diffuse (33%).

The intestinal type of sporadic gastric adenocarcinoma has a hallmark

progression from normal gastric epithelium to atrophic to chronic atrophic gastritis
(typically due to Helicobacter infection) to intestinal metaplasia to dysplasia to
cancer.

This

assumption

supported

by

electron

microscopic

and

immunohistochemical studies.

Their degree of differentiation ranges widely and correlates inversely with

tumor size. In the better differentiated tumors, most of the cells are columnar and
mucin secreting. Poorly differentiated variants have a predominantly solid pattern.
Exceptionally the better differentiated tumors are ciliated. The amount of mucin
production is highly variable, when abundant; it is often accompanied by
calcification.

10

Diffuse type adenocarcinoma are best represented by the tumour type

clinically known as linitus plastica and currently designated as signet ring (adeno)
carcinoma. The gross alteration usually begins in the prepyloric area. Pyloric
obstruction often develops, as the wall of the stomach becomes thickened and
rigid. Sections of the wall show marked submucosal fibrosis, with or without
mucosal ulceration. The muscle is hypertrophied and segmented by the presence
of the parallel, grayish white, longitudinal lines that give it a comb like
appearance. The lines are continuous with foci of subserosal thickening.
Microscopically a diffuse growth of malignant cells is seen, associated with
extensive fibrosis and inflammation. Often the entire wall is involved.

Although an intramural type of signet ring carcinoma occurs in many cases

of this entity the mucosa is less affected than the deeper layers. Glandular
formations are rare and most tumour cells grow individually. Most of the mucin
produced as intra-cytoplasmic, resulting in the typical signet ring appearance.
There are few malignant tumours in the body that are more likely to be missed on
microscopic examination than this type of gastric carcinoma. Over the years
specimens have been seen from the stomach wall, lymph nodes, mesentery, pelvic
peritoneum and ovary that were initially misinterpreted as a begin process because
of the inconspicuousness of the tumour cell and the marked degree of
inflammatory and desmoplastic reaction. The tumour may also simulate
lymphoma because of its diffuse pattern of growth and the round shape of the cells
and their nuclei. 11

11

Figure 2 Photomicrographs of gastric adenocarcinoma. A, Gastric adenocarcinoma intestinal

type (H&E, 25). B, Gastric adenocarcinoma intestinal type (H&E, 400). C, Gastric
adenocarcinoma diffuse type (H&E, 25). D, Gastric adenocarcinoma diffuse type (H&E,
400). Arrows on signet ring cells.

Table 1 -- Lauren Classification System

INTESTINAL

DIFFUSE

Environmental

Familial

Gastric Atrophy, metaplasia

Blood group A

Men>Women

Women>men

Increasing incidence with age

Younger age group

Gland formation

Poorly differentiated, signet ring cells

Hematogenous spread

Transmural/lymphatic spread

Microsatellite instability, APC gene Decrease E-cadherin

mutations
p53, p16 inactivation

P53, p16 inactivation

12

Broder's classification of gastric cancer grades tumors histologically from 1

(well-differentiated) to 4 (anaplastic). Bearzi and Ranaldi have correlated the
degree of histologic differentiation with the gross appearance of 41 primary gastric
cancers seen on endoscopy. Ninety percent of protruding or superficial cancers
were well differentiated (Broder's grade 1), whereas almost half of all ulcerated
tumors were poorly differentiated or diffusely infiltrating (Broder's grades 3 and
4).8

The WHO classification, 2000 classifies gastric cancer into

Adenocarcinoma- intestinal and diffuse types,

Papillary adenocarcinoma,
Tubular adenocarcinoma,
Mucinous adenocarcinoma,
Signet ring cell adenocarcinoma,
Adenosquamous adenocarcinoma,
Squamous cell carcinoma,
Small cell carcinoma,
Undifferentiated carcinoma and Others.11,12

13

Classification of Esophagogastric Junction Cancers

Siewert and Stein have developed a classification system for adenocarcinoma

of the esophagogastric junction. Now commonly referred to as the Siewert
classification, this system recognizes three distinct clinical entities that arise
within 5 cm of the junction of the tubular esophagus and the stomach:

Type 1: Adenocarcinoma of the distal esophagus, which usually arises

from an area with specialized intestinal metaplasia of the esophagus (i.e.,
Barrett's esophagus) and may infiltrate the esophagogastric junction from
above.

Type II: Adenocarcinoma of the cardia, which arises from the epithelium of
the cardia or from short segments with intestinal metaplasia at the
esophagogastric junction

Type III: Adenocarcinoma of the subcardial stomach, which may infiltrate

the esophagogastric junction or distal esophagus from below

14

The assignment of tumors to one of these subtypes is based on morphology

and the anatomic location of the epicenter of the tumor. Classification can be
performed based on the results of contrast radiography, endoscopy, CT, and
operative findings. The Siewert classification has important therapeutic
implications.13,14

Histochemical, immunohistochemical and electron microscopic features

The secretory product of most gastric adenocarcinoma(esp those of the

intestinal type) is an acid mucosubstance, easily detected with Mayers
mucicarmine, Alcian blue or colloidal iron stains and having feature analogous to
the those of intestinal type mucins. Various alterations in the syalidation of the
mucins occur and can be detected histochemically or immunohistochemically.

At the immunohistochemical level, the main mucin types expressed are

MUC1 for the intestinal type, MUC5AC for the diffuse and MUC2 for mucinous
types. There is also an interesting relationship between mucin type and is
prevalent with carcinoma of the antrum whereas MUC2 is expressed in greater
amounts in carcinoma of the cardia.

In terms of immunomarkers reactivity of gastric adenocarcinoma for

keratin, epithelial membrane antigen and CEA is the rule.11

15

RISK FACTORS
Inherited Susceptibility

Case-control studies have observed consistent, up to threefold, increases in

risk for gastric cancer among relatives of patients with gastric cancer. Studies of
monozygotic twins have even shown a slight trend toward increased concordance
of gastric cancers compared with dizygotic twins. Large families with an
autosomal dominant, highly penetrant inherited predisposition for the development
of gastric cancer are rare. However, early-onset diffuse gastric cancers have been
described and linked to the E-cadherin/CDH1 locus on 16q and associated with
mutations in this gene. This seminal finding has been confirmed in other studies
with gastric cancers at a relatively high (67% to 83%) penetrant rate. Thus, Ecadherin mutation testing should be considered in the appropriate clinical setting.
In fact, prophylactic gastrectomy should be considered strongly in families with
germ line E-cadherin mutation even without gross mucosal abnormalities by
endoscopic examination of the stomach.

Hereditary nonpolyposis colon cancer (HNPCC) involves germ line

mutations of DNA mismatch repair genes. Gastric adenocarcinoma may be
observed in families with HNPCC. Gastric cancers have also been noted to occur
in patients with familial adenomatous polyposis and Peutz-Jeghers syndromes.14

16

Table 2 - Genetic Abnormalities in Gastric Cancer

Abnormalities
Deletion/suppression

Gene
p53
FHIT
APC
DCC
E-cadherin
Amplification/overexpression COX
HGF/SF
VEGF
c-met
AIB-1
- catenin
k-sam
Ras
c-erb B2
Microsatellite instability
DNA aneuploidy

Approximate Frequency %
6070
60
50
50
<5
70
60
50
45
40
25
20
10-15
5-7
25-40
60-75

Fig.3 The role of Helicobacter Pylori

17

Role of helicobacter pylori

As a commensal organism, Helicobacter pylori infection is widely
prevalent throughout the world. Despite its classification by the World Health
Organization as a class I carcinogen, infection with H. pylori does not typically
lead to gastric cancer. This underscores the importance of other factors, such as
virulence, environmental, and host factors, as well as genetic polymorphisms (e.g.,
in interleukin-1, a potent inhibitor of acid secretion). The blood group A
phenotype has been reported to be associated with gastric cancers. Helicobacter
pylori may adhere to the Lewis Blood Group antigen, indicating a factor for
increased risk for gastric cancer. Small variant alleles of a mucin gene, Muc1,
were found to be associated with gastric cancer patients when compared with a
blood donor control population.

The risk of gastric cancer in patients with chronic H. pylori infection is

increased about threefold. When compared to uninfected patients, patients with a
history of gastric ulcer are more likely to develop gastric cancer , and patients with
a history of duodenal ulcer are at decreased risk for gastric cancer. This may be
due to the fact that some patients develop antral-predominant disease
(predisposing to duodenal ulcer and somehow protecting against gastric cancer),
while other patients develop corpus-predominant gastritis, resulting in
hypochlorhydria and somehow predisposing to gastric ulcer and gastric cancer.

18

Recently, it has been demonstrated that bone marrowderived stem cells

play a key role in the pathogenesis of gastric adenocarcinoma in patients with
chronic H. pylori infection. However, it must be recognized that gastric
adenocarcinoma is a multifactorial disease. Not all patients with gastric cancer
have H. pylori, and there are some geographic areas with a high prevalence of
chronic H. pylori infection and a low prevalence of gastric cancer (the "African
enigma"). Finally, H. pyloriinfected patients seem to be at decreased risk for the
development of adenocarcinoma of the distal esophagus and cardia region.
Perhaps the corporeal gastritis decreases acid secretion, creating a less damaging
refluxate and thus reducing the risk for Barrett's esophagus, the precursor lesion
for these tumors.14

Epstein Barr Virus

Epstein-Barr virus (EBV) has been found to be associated with a type of

gastric carcinoma (EBVaGC). EBV may be a factor initiating EBVaGC. EBV may
infect the surface epithelium of the stomach through the reactivated EBV-carrying
lymphocytes. Using PCR and EBER1 in situ hybridization, EBVaGC (definitely
amplifiable EBV-DNA and positive EBER1-signal in the nuclei of carcinoma
cells) was found in 8 of 72 gastric carcinomas (11%). EBVaGC was found in the
cardia (4/8) or body (4/8) of the stomach, and consisted of 7 advanced and 1
intramucosal carcinoma.

19

Patients with EBVaGC showed high titers of anti-VCA IgG (8/8), antiVCA IgA (2/8) and anti-EA IgG (7/8) antibodies just before surgery. Anti-EBV
antibodies or EBER1 in situ hybridization may help to identify patients at high
risk for EBVaGC stomach.15
Diet

Diet is generally accepted as the main factor in gastric cancer etiology.

There is, however, no general agreement on the specific components of the diet
supposedly responsible for gastric cancer. The geographic distribution of the
disease shows marked inter-country contrasts but there are many examples of
culturally-divergent populations inhabiting the same land but having contrasting
gastric cancer rates. Migrants from high-risk areas acquire the low rates of
adoptive countries. Culture, not race or geography, appears as the main
determinant of gastric-cancer risk. Diet is the cultural component which offers the
most logical explanation of inter-population contrasts.

The gastric-cancer diet has been characterized as follows

(a) Low in animal fat and animal proteins
(b) High in complex carbohydrates
(c) A substantial proportion of the protein obtained from vegetable sources,
mostly grains and tubers
(d) Low in salads and fresh, green, leafy vegetables
(e) Low in fresh fruits, especially citrus
(f) High in salt.

20

In addition, a controversial role of nitrates has been reported.16 Nitrates are

converted to carcinogenic nitrites by bacteria. Such bacteria may be introduced
through consumption of partially decayed foods, a practice that is more common
in the lower social economic strata worldwide.2

Humans are exposed to a wide range of N-nitrosocompounds (NOCs) from

diet, tobacco smoking, work place and drinking water, which are the major source
of exposure in the general population. Preformed exogenous nitrosamines are
found mainly in cured meat products, smoked preserved foods, foods subjected to
drying by additives such as malt in the production of beer and whiskey, pickled
and salty preserved foods.

Available data suggest that nitrosamines are found more frequently and at
higher concentration in Asian foods than in Western foods. On the other hand,
nitrosamines are formed endogenously from nitrate and nitrite. Although the levels
have reduced during the last 20 years, sodium nitrites are still widely used as food
preservatives in cured meat products. Nitrite is also formed in the human body
from oral reduction of salivary nitrate. Vegetables and water are the main sources
of nitrate intake. Nitrites are transformed into nitric oxide by gastric acid-catalyzed
formation, which acts as nitrosating agent of amines and amides, as consequence
of NOC. Under chronic inflammatory conditions, such as precancerous conditions
of gastric cancer (GC) and esophageal cancer (OC), nitrosating agents are
overproduced.17

21

Excessive salt intake as a factor has epidemiologic and experimental

support.16 A recent case-control study in Mumbai found that consumption of dried
fish increased the risk while green tea consumption decreased the risk of having
stomach cancer. A prospective case-control study from Trivandrum evaluated
dietary risk factors for stomach cancer and found that high consumption of rice,
spicy food, chili , and high-temperature food increased the risk of developing
stomach cancer.

Fried foods are associated with higher rates of cancer due in part to the
production of carcinogenic or mutagenic heterocyclic amines (HA) during the
cooking process. Case-control and prospective studies have reported an increased
risk of stomach, colon, and bladder cancers with moderate to heavy consumption
of fried foods. The use of the spice turmeric is associated with a reduced risk of
stomach cancer, in part because of its protective effect against the carcinogenic
bacterium H. pylori, a major risk factor for stomach cancer.18

Conversely, the consumption of raw vegetables, citrus fruits, and high-fiber

breads is associated with a lower risk for gastric cancer. The ascorbic acid and carotene found in fruits and vegetables act as antioxidants, whereas ascorbic acid
can also prevent the conversion of nitrates to nitrites.2

In a carefully conducted case-control study at Chennai, the authors have

identified alcohol consumption as an independent risk factor.19 Studies of the

22

relation between alcohol consumption and the risk of GCA have been largely
inconclusive, and case-control studies from India have not identified alcohol
intake as an independent risk factor for GCA in India.20Beer specimens obtained
from several Indian cities in South India have been shown to contain Nnitrosodimethylamine in large amounts,21 and this may be an important factor for
the high risk of GCA associated with alcohol consumption in our part of the
country. 19

PRECANCEROUS LESIONS

Atrophic gastritis

This is a histological diagnosis. The main features are a variable degree of

inflammation, atrophy of gastric glands, and often associated intestinal metaplasia,
which changes are more commonly found in the antrum than in the body or the
fundus of the stomach.

Patients with atrophic gastritis are statistically at increased risk from cancer
of the stomach but precise measurement of this risk is yet to be determined. There
is a significant geographical relationship between areas of high frequency for
gastric carcinoma and the incidence of atrophic gastritis and intestinal metaplasia.

23

Within the histological spectrum of atrophic gastritis intestinal metaplasia

is the most sensitive risk indicator. Most gastric cancers develop on a basis of
atrophic gastritis, but the epithelial change which statistically most predisposes to
malignancy is intestinal metaplasia.

Gastric ulcer

The incidence of so-called 'ulcer-cancer', that is, carcinoma developing in a

pre-existing peptic ulcer, has been debated hotly for many years. There are two
essential criteria for the diagnosis: first, there must be definite evidence of a preexisting ulcer (complete destruction of a zone of muscle, dense fibrous tissue in
the floor of the lesion, endarteritis and thrombophlebitis in surrounding vessels,
fusion of muscle coats and muscularis mucosae at the edge of the lesion) and,
second, there must be definite evidence of malignant change at the edge of the
ulcer quite distinct from any attempt at epithelial regeneration.

In any assessment one must remember that chronic ulcer and cancer may
coexist in a stomach without necessarily being causally related; studies in Japan
suggest that gastric ulcer and gastric cancer also have a different geographic
distribution. Ulcer-cancers undoubtedly do occur, particularly when the ulcer is
chronic, but the incidence of cancer developing in a proven peptic ulcer and the
presence of unequivocal evidence of previous peptic ulcer at the site of a proven
carcinoma are both probably not more than 1 %.

24

Pernicious anemia
There is statistical and histological evidence that patients with pernicious
anemia are at increased risk from cancer of the stomach. True adenomatous polyps
and carcinoma of the stomach have been reported to be three to four times more
common in patients with pernicious anemia than in the general population
although a recent study suggests that this may be an underestimate, since some
patients with carcinoma but without overt pernicious anemia are in a 'prepernicious anemia stage'.

Moreover, it appears that the carcinomas are mostly found in the body or
the fundus of the stomach rather than in the pyloric antrum, which is where most
gastric cancers are seen. 22

Gastric stumps

Balfour first reported a correlation between prior gastric surgery for benign
disease and the subsequent development of gastric cancer in 1922. Subsequent
meta-analyses support the conclusion that there is an increased risk for gastric
remnant cancer in patients with prior partial gastrectomy. However, the risk is only
observed after a latency of 15 years and is increased in patients operated on for
gastric but not duodenal ulcers.

25

The incidence of malignancy ranges from 2% to 6% in gastric remnants,

and a variety of causative factors have been proposed to include alkaline duodenal
gastric reflux as well as increased N-nitroso compounds secondary to bacterial
overgrowth. The development of atrophic gastritis along with gastritis cystica
profunda can be associated with dysplasia in 5% of patients, for which
surveillance endoscopy is indicated.2

Gastric stump carcinomas usually develop close to the anastomosis on the

gastric side. Polypoid lesions are common in the same area, but their significance
has not yet been established; many are hyperplastic or regenerative polyps, and
others may be pseudo polyps resulting from the construction of the anastomosis.22

Gastric polyps

Polypoid lesions of the stomach can be divided into those with and without
malignant potential. The common ones, hyperplastic or regenerative polyps, have
insignificant malignant potential. Polypoid lesions in which the epithelium shows
dysplasia (which are called adenomas or borderline lesions by some) have a
significant capacity for malignant change. It is exceptional for gastric adenomas to
have a stalk, particularly a long one, and most of them are sessile. They can be
very flat, slightly elevated tumours and are more often single than multiple.

26

Most gastric adenomas are of the intestinal type, which suggests that they
have developed on a basis of atrophic gastritis and intestinal metaplasia. Gastric
adenomas are uncommon but have a very significant potential for malignant
change.

It is possible that only a small minority of gastric cancers arise from

previously benign adenomas. The diagnosis of benign adenoma must be made
with care, because multiple sections through the tumour may show signs of
intramucosal carcinoma.

Mentriers Disease

There is a growing list of case reports of carcinoma of the stomach

complicating Menetrier's disease. The statistical risk of cancer in this disease is not
known, and anyway the diagnosis of Menetrier's disease is difficult to define both
clinically and pathologically.

There are descriptions of both intestinal metaplasia and epithelial dysplasia

of gastric epithelium in some of the reports.22

27

CLINICAL MANIFESTATIONS

Most patients who are diagnosed with gastric cancer in the United States
have advanced stage III or IV disease at the time of diagnosis. The most common
symptoms are weight loss and decreased food intake due to anorexia and early
satiety. Abdominal pain (usually not severe and often ignored) also is common.
Other symptoms include nausea, vomiting, and bloating. Acute GI bleeding is
somewhat unusual (5%), but chronic occult blood loss is common and manifests
as iron deficiency anemia and heme-positive stool. Dysphagia is common if the
tumor involves the cardia of the stomach. Paraneoplastic syndromes such as
Trousseau's

syndrome

(thrombophlebitis),

acanthosis

nigricans

(hyperpigmentation of the axilla and groin), or peripheral neuropathy are rarely

present.

Physical examination usually is normal. Other than signs of weight loss,

specific physical findings usually indicate incurability. A focused examination in a
patient in whom gastric cancer is a likely part of the differential diagnosis should
include an examination of the neck, chest, abdomen, rectum, and pelvis. Cervical,
supraclavicular (on the left referred to as Virchow's node), and axillary lymph
nodes may be enlarged, and today can be sampled in the office with fine-needle
aspiration cytology. There may be a metastatic pleural effusion, or aspiration
pneumonitis in a patient with vomiting and/or obstruction.

28

An abdominal mass could indicate a large (usually T4 incurable) primary

tumor, liver metastases, or carcinomatosis (including Krukenberg's tumor of the
ovary). A palpable umbilical nodule (Sister Joseph's nodule) is pathognomonic of
advanced disease, or there may be evidence on exam of malignant ascites.1
Gastric carcinoma may also present as multiple cutaneous nodules.23

Rectal exam may reveal heme-positive stool and hard nodularity

extraluminally and anteriorly, indicating so-called drop metastases, or rectal shelf
of Blumer in the pouch of Douglas.1

Preoperative Evaluation

Radiologic examination of the stomach can identify advanced gastric

cancers; however it is less accurate than endoscopy for identification of early
gastric cancer. All ulcers identified by x-ray examination should be referred for
endoscopic biopsy.

Radiologic criteria that suggest a benign ulcer include radiating folds and a
normal-appearing mucosal surface around the crater. Linitus plastica is suggested
by radiologic studies that demonstrate a nondistensible stomach.

29

Endoscopy

When gastric cancer is suspected based on history and physical

examination, flexible upper endoscopy is the diagnostic modality of choice.
Although double-contrast barium upper GI radiography is cost-effective with 90%
diagnostic accuracy, the inability to distinguish benign from malignant gastric
ulcers makes endoscopy preferable. During endoscopy, multiple biopsy samples
(seven or more) should be obtained around the ulcer crater to facilitate histologic
diagnosis. When multiple biopsy specimens are taken, the diagnostic accuracy of
the procedure approaches 98%.

The addition of direct brush cytology to multiple biopsy specimens may

increase the diagnostic accuracy of the study. Additionally, the size, location, and
morphology of the tumor should be noted and other mucosal abnormalities
carefully

evaluated.

In

select

patients

with

advanced

disease,

esophagogastroduodenoscopy provides a means for palliation through the use of

laser ablation, dilation, or tumor stenting. Although not included in the National
Comprehensive Cancer Network guidelines for the evaluation of gastric
adenocarcinoma, some centers are using endoscopic Ultrasonography (EUS) to
assist in the staging of this disease. EUS can gauge the extent of gastric wall
invasion as well as evaluate local nodal status. However, EUS cannot reliably
distinguish tumor from fibrosis; therefore, it is not a good modality for evaluating
response to therapy.2

30

CT scan

Computed tomography (CT) scans of the chest and abdomen are the
primary imaging modalities for preoperative staging of stomach. In stomachs that
are well distended with contrast, wall thickness of >2 cm indicates transmural
extension of the tumor. Evidence of direct invasion of perigastric fat, diaphragm,
pancreas, transverse colon, and left lobe of the liver should be sought. Metastases
to the liver, lung, and other organs can also be documented.

For gastric adenocarcinoma overall accuracy of preoperative CT scans

ranges from 61 to 72%.

23

In women, a pelvic CT scan or ultrasound is also

recommended. CT of the chest may be needed for proximal gastric cancers The
major limitations of CT are in the evaluation of early gastric primaries and in the
detection of small (<5 mm) metastases in the liver or on peritoneal surfaces.2 CT
scans are particularly unreliable in assessing regional lymph nodes and invasion of
adjacent organs, resulting in under staging of the disease.

CT scans may also over stage gastric adenocarcinoma, resulting in labeling

the cancer as unresectable when in fact the tumor may be resectable. Careful
review of preoperative CT scans by the gastroenterologist, surgeon, and
radiologist is necessary before making a decision regarding resectability. 2

31

Positron Emission Tomography

Whole-body PET scanning uses the principle that tumor cells preferentially
accumulate positron-emitting

18

F-fluorodeoxyglucose. This modality is most

useful in the evaluation of distant metastasis in gastric cancer but can also be
useful in locoregional staging. PET scan is most useful when combined with spiral
CT (PET-CT) and should be considered before major surgery in patients with
particularly high-risk tumors or multiple medical comorbidities.23

Laparoscopy

Because of the inaccuracy of CT and other modalities for the detection of

macrometastases smaller than 5 mm on the peritoneal surface or liver, laparoscopy
is recommended as the next step in the evaluation of patients with locoregional
disease. Laparoscopy can detect metastatic disease in 23% to 37% of patients
judged to be eligible for potentially curative resection by current-generation CT
scanning.

Laparoscopy

may

therefore

improve

palliation

by

avoiding

nontherapeutic laparotomy in patients presumed to have localized gastric cancer.

The addition of laparoscopic ultrasonography may increase the sensitivity of
laparoscopic staging in gastric cancer as it has in other abdominal malignancies.

32

Cytologic analysis of peritoneal fluid or of fluid obtained by peritoneal

lavage may reveal the presence of free intraperitoneal gastric cancer cells,
identifying patients with otherwise occult carcinomatosis. More sensitive methods
of detecting free intraperitoneal gastric cancer cells, such as immunostaining and
reverse-transcriptase polymerase chain reaction for carcinoembryonic antigen
(CEA) messenger RNA, are under investigation.2

STAGING

Many staging systems have been proposed for gastric adenocarcinoma. A

basic understanding of the older systems is necessary to understand the literature.
The pathologic staging system currently in use worldwide is the AJCC TNM
staging system. The TNM system can adequately stratify patients into distinct
groups with different risks for tumor-related death. A major revision occurred in
the AJCC staging system for gastric cancer in 1997 when nodal status
stratification was changed from location of nodes to number of positive nodes. In
the current staging system, a minimum of 15 nodes must be evaluated for accurate
staging. Nodal staging is then determined by the number of positive nodes, with
pN1 reflecting 1 to 6 positive nodes, pN2 designating 7 to 15 positive nodes, and
pN3 more than 15 positive nodes. 2

33

TNM STAGING OF GASTRIC CARCINOMA

T: Primary tumor
Tis
Carcinoma in situ; intraepithelial tumor without invasion of lamina propria
T1
T2
T3

Tumor invades lamina propria or submucosa

Tumor invades muscularis propria or subserosa
Tumor penetrates serosa (visceral peritoneum) without invasion of adjacent
structures
T4
Tumor invades adjacent structures
N: Regional lymph node
N0
No regional lymph node metastasis
N1
Metastasis in 1 to 6 regional lymph nodes
N2
Metastasis in 7 to 15 lymph nodes
N3
Metastasis in more than 15 regional lymph nodes
M: Distant metastasis
M0
No distant metastasis
M1
Distant metastasis

Table 3 TNM staging of gastric carcinoma

STAGE
0
IA
IB
II

IIIA

IIIB
IV

T
Tis
T1
T1
T2
T1
T2
T3
T2
T3
T4
T3
T4
T1-3
Any T

N
N0
N0
N1
N0
N2
N1
N0
N2
N1
N0
N2
N1-3
N3
Any N

M
M0
M0
M0
M0
M0
M0
M0
M0
M0
M0
M0
M0
M0
M1

Table 4: Staging of gastric carcinoma

34

Fig .4 T Stage defined by depth

of penetration into gastric wall

Resection classification
The term R status was first described by Hermanek in 1994 and is used to
describe the tumor status after resection. R0 describes a microscopically marginnegative resection, in which no gross or microscopic tumor remains in the tumor
bed. R1 indicates removal of all macroscopic disease, but microscopic margins are
positive for tumor. R2 indicates gross residual disease. Because the extent of
resection can influence survival, some authors include this R designation to
complement the TNM system. Long-term survival can be expected only after an
R0 resection; therefore, a significant effort should be made to avoid R1 or R2
resections.

Knowledge of the older staging systems and the Japanese system is crucial
to the understanding of the debate regarding lymphadenectomies for gastric
cancer. The Japanese Classification for Gastric Carcinoma (JCGC) staging system
was designed to describe the anatomic locations of nodes removed during
gastrectomy. Sixteen distinct anatomic locations of lymph nodes are described ,
with the recommendation for nodal basin dissection dependent on the location of
the primary. The lymph node stations or echelons are numbered and then further
classified into groups of echelons that correspond to the location of the primary
and reflect the likelihood of harboring metastases . The presence of metastasis to
each lymph node group then determines the N classification. For example,
metastases to any of the group 1 lymph nodes in the absence of disease in more
distant lymph node groups is classified as N1. 2

35

Table 5 Japanese Gastric Cancer Association Staging System for Gastric Cancer
TUMOR STAGE
T1 Tumor invasion of mucosa and/or muscularis mucosa (M) or submucosa (SM)
T2 Tumor invasion of muscularis propria (MP) or subserosa (SS)
T3 Tumor penetration of serosal (SE)
T4 Tumor invasion of adjacent structures (SI)
TX Unknown
NODAL STAGE
N0 No evidence of lymph node metastasis
N1 Metastasis to group 1 lymph nodes, but no metastasis to groups 2 to 3 lymph
nodes
N2 Metastasis to group 2 lymph nodes, but no metastasis to group 3 lymph nodes
N3 Metastasis to group 3 lymph nodes
NX Unknown
HEPATIC METASTASIS STAGE (H)
H0 No liver metastasis
H1 Liver metastasis
HX Unknown
PERITONEAL METASTASIS STAGE (P)
P0 No peritoneal metastasis
P1 Peritoneal metastasis
PX Unknown
PERITONEAL CYTOLOGY STAGE (CY)
CY0 Benign/indeterminate cells on peritoneal cytologya
CY1 Cancer cells on peritoneal cytology
CYXPeritoneal cytology was not performed
OTHER DISTANT METASTASIS (M)
M0 No other distant metastases (although peritoneal, liver, or cytological metastases
may be present)
M1 Distant metastases other than the peritoneal, liver, or cytological metastases
MX Unknown
STAGE GROUPING
N0
N1
N2
N3
T1 IA
IB
II
T2 IB
II
IIIA
T3 II
IIIA
IIIB
IV
T4 IIIA
IIIB
H1, P1, CY1, M1
a
Cytology felt to be suspicious for malignancy should be classified as CY0.

36

Fig 5 Lymph node station numbers as defined by Japanese Cancer Association

37

LOCATION OF PRIAMRY TUMOUR IN

THE STOMACH
LYMPH NODE STATION(No)

DESCRIPTION

Right paracardial

Upper third

Middle third

Lower third

Left paracardial

Lesser curvature

4sa

Short gastric

4sb

Left gastroepiploic

4d

Right gastroepiploic

Suprapyloric

Infrapyloric

Left gastric artery

8a

Anterior comm. hepatic

8p

Posterior comm. hepatic

Celiac artery

10

Splenic hilum

11p

Proximal splenic

11d

Distal splenic

12a

Left hepatoduodenal

12b,p

Posterior hepatoduodenal

13

Retropancreatic

14v

Superior mesenteric vein

14a

Superior mesenteric artery

15

Middle colic

16al

Aortic hiatus

16a2,b1

Para-aortic, middle

16b2

Para-aortic, caudal

M, lymph nodes regarded as distant metastasis

Table 6 - Grouping of Regional Lymph Nodes (Groups 1-3) by Location of Primary
Tumor According to the Japanese Classification of Gastric Carcinoma

38

Spread of carcinoma of the stomach

No better example of the various modes by which carcinoma spreads can

be given than the case of stomach cancer. It is important to note that this distant
spread is unusual before the disease spreads locally and distant metastases are
uncommon in the absence of lymph node metastases. The intestinal and diffuse
types of gastric cancer spread differently. The diffuse type spreads via the
submucosal and subserosal lymphatic plexus and it penetrates the gastric wall at
an early stage.

Direct spread

The tumour penetrates the muscularis, serosa and ultimately adjacent

organs such as the pancreas, colon and liver.

Lymphatic spread

This is both by permeation and emboli to the affected tiers (see below) of
nodes. This may be extensive, the tumour even appearing in the supraclavicular
nodes (Trosiers sign). Unlike malignancies such as breast cancer, nodal
involvement does not imply systemic dissemination.

39

Blood-borne metastases

This occurs first to the liver and subsequently to other organs including
lung and bone. This is uncommon in the absence of extensive nodal disease.

Trans peritoneal spread

This is a common mode of spread once the tumour has reached the serosa
of the stomach and indicates incurability. Tumours can manifest anywhere in the
peritoneal cavity and commonly give rise to ascites. Advanced peritoneal disease
may be palpated either abdominally or rectally as a tumour shelf.

The ovaries may sometimes may be the sole site of transcoelomic spread
(Krukenbergs tumours). Tumour may spread via the abdominal cavity to the
umbilicus (Sister Josephs nodule). 25

40

TREATMENT OF LOCALIZED DISEASE

STAGE I DISEASE (EARLY GASTRIC CANCER) Classification and Risk

for Nodal Metastases

The Japanese Research Society for Gastric Cancer has classified early
gastric cancers (EGC) based on endoscopic criteria first established by the
Japanese Endoscopy Society for the description of T1 tumors.

The current classification system is used for both in situ and invasive
tumors and categorizes tumors based on endoscopic findings as follows:

Figure 6 . Japanese classification system for early gastric cancer. In the combined
superficial types, the type occupying the largest area should be described first,
followed by the next type (e.g., IIc + III). Type 0I and Type 0IIa are distinguished as
follows: Type 0I: The lesion has a thickness of more than twice that of the normal
mucosa. Type 0IIa: The lesion has a thickness up to twice that of the normal mucosa.

41

Considering the risk for lymph node metastasis is important when

evaluating treatment options for patients with EGC. The frequency and anatomic
distribution of nodal disease are related to the depth of tumor invasion. 10

Treatment options for patients with EGC include

-

Endoscopic Mucosal Resection (EMR),

Limited surgical resection,

Gastrectomy.

Endoscopic Mucosal Resection

This approach involves the submucosal injection of fluid to elevate the

lesion and facilitate complete mucosal resection under endoscopic guidance. Only
patients with tumors that have extremely low metastatic potential should be
offered EMR.

These are generally well-differentiated, superficial type IIa or IIc lesions

smaller than 3 cm in diameter and located in an easily manipulated area. Tumors
invading the submucosa are at increased risk for metastasizing to lymph nodes and
are not usually considered candidates for EMR.

42

Limited Surgical Resection

Given the low rate of nodal involvement for patients with EGC, limited
resection may be a reasonable alternative to gastrectomy for some patients with
early EGC. There are no well-accepted pretreatment criteria for selection of
patients for limited resection. Based on the existing pathology data, patients with
small (less than 3 cm) intramucosal tumors and those with nonulcerated
intramucosal tumors of any size may be candidates for EMR or limited resection.
Surgical options for these patients may include gastrectomy with local excision.

Gastrectomy

Gastrectomy with lymph node dissection should be considered for patients

with EGC who cannot be treated with EMR or limited surgical resection and/or
patients who have intramucosal tumors with poor histologic differentiation or size
greater than 3 cm or who have tumor penetration into the submucosa or beyond.
Gastrectomy with lymph node dissection allows for adequate pathologic staging
and local therapy for these higher-risk patients.
There is no consensus on the extent of lymphadenectomy that should be
performed as part of gastrectomy for EGC. Dissection of level I lymph nodes is a
reasonable minimum standard at this time.

43

STAGE II AND STAGE III DISEASE

Surgery

Surgical resection is the cornerstone of treatment for patients with localized

gastric cancer. However, for stages II and III disease, surgery is necessary but
often not sufficient for cure. The general therapeutic goal is to achieve a microand macroscopically complete resection (R0). 10

Extent of Gastric Resection

There is no evidence that an extended gastric resection above and beyond

complete clearance of the primary tumor improves survival; i.e., total gastrectomy
does not improve survival over distal or proximal gastrectomy, provided that the
tumor is removed completely with negative transection margins (R0 resection).
This has been confirmed in a number of randomized trials. The extent of
the gastrectomy therefore is site-dependent and focuses on complete removal of
the gastric carcinoma with preferably a 4- to 5-cm margin from the gross edge of
the tumor. Clearly, anatomic limitations influence this margin because in antral
lesions close to or involving the pylorus, only a limited portion of the duodenum
can be removed.

44

In similar fashion, a lesser extent of uninvolved esophageal margin may be

acceptable provided complete histologic resection is possible.
In patients with a distal lesion, a distal subtotal gastrectomy is performed
essentially regardless of T stage. For proximal gastric cancers and true GE
junction cancers (Siewert types II and III), sub diaphragmatic proximal
gastrectomy with esophagogastrectomy, can be liberally used whereas some prefer
total gastrectomy for any lesion not in the antrum.

For midbody or more extensive lesions, total gastrectomy is required,

whereas for more distal lesions, a subtotal gastrectomy is the preferred approach.
It is important to emphasize that in most studies there is an increase in morbidity
and mortality when total gastrectomy is performed over distal subtotal
gastrectomy. Since long-term survival is not improved by the more extensive
resection, this is a further factor in favor of subtotal resection, provided that an R0
resection can be obtained.
Proximal resections, however, appear to have similar perioperative
morbidity and mortality to total gastrectomy.

Extended organ resection is reserved for patients with apparently nodenegative T4 lesions, in which complete resection requires resection of the invaded
portions of the diaphragm, pancreas, spleen, adrenal gland, or colon.27

45

Extent of Lymphadenectomy

The dialogue surrounding lymphadenectomy involves at least two

important issues: (1) staging removal and histopathologic analysis of an adequate
number of lymph nodes, and (2) therapy determining if some forms of
lymphadenectomy are therapeutic for patients with gastric cancer.
The current AJCC staging system (sixth edition) requires analysis of 16 or more
lymph nodes to assign a pathologic N stage.

Adjuvant Therapy

The term adjuvant therapy is best used to describe additional treatment in

an attempt to increase cure rates in patients who have already undergone a
potentially curative resection. For gastric cancer, an R0 surgical procedure, in
which all gross disease has been removed, the margins of resection are
microscopically negative, and no distant metastases were found, is required before
adjuvant therapy is considered. Resections that leave microscopic or gross residual
disease are not adjuvant treatment, but rather therapy of known residual cancer.
The term perioperative chemotherapy (or neoadjuvant chemotherapy) involves the
use of systemic treatment before definitive, potentially curative surgery.

46

Adjuvant Postoperative Systemic Therapy

Adjuvant postoperative systemic chemotherapy has not shown a significant
advantage over surgery alone.

Postoperative Adjuvant Intraperitoneal Chemotherapy

Peritoneal recurrence is a common component of the failure pattern for
patients with gastric cancer. The rationale for the use of intraperitoneal treatment
is based on the pharmacokinetic observation that drug concentrations within the
peritoneal cavity after intraperitoneal administration are much higher than those
achievable intravenously or orally.

For gastric cancer, an increasing number of reports have been published in

which immediate postoperative intraperitoneal therapy was given after potentially
curative resection. However, no definitive conclusions can yet be drawn regarding
the effectiveness of intraperitoneal postoperative chemotherapy in this setting.

Immunochemotherapy
The

use

of

adjuvant

immunostimulants

(either

protein-bound

polysaccharide (PSK) or a Streptococcus pyrogenes preparation, OK432) given in

association with cytotoxic chemotherapy has been studied, however larger studies
that are adequately powered would be necessary to definitively evaluate this
approach.

47

Perioperative (Neoadjuvant) Chemotherapy

Perioperative (pre- and postoperative) chemotherapy, also known as
neoadjuvant chemotherapy, is an attractive concept in gastric cancer because many
patients, particularly Western patients, have locally advanced tumors at diagnosis
(T3 or T4, or obvious lymph node involvement).

Such patients are not only at substantial risk for distant metastasis, but local
extent of the tumor may make an R0 resection difficult.

There are two goals to perioperative treatment: reduce the stage of the
primary tumor to increase the likelihood that a R0 resection can be performed, and
begin at an early time to treat micrometastatic disease.

Adjuvant Radiation and Chemoradiation Therapy

Most of the studies that have evaluated radiation therapy as an adjuvant
have used concomitant 5-FU chemotherapy. There was a significant improvement
in survival with the combination of 5-FU and radiation compared with radiation
alone.

48

Technical Treatment-Related Issues

Surgery
Beginning with laparoscopy allows for careful intraoperative staging of
disease. Inspection for the presence of ascites, hepatic metastases, peritoneal
seeding, disease in the pelvis (such as a metastasis), or ovarian involvement should
be performed. Once distant metastases have been ruled out, depending on the
location of the lesion, a bilateral subcostal incision or a midline abdominal
incision can be used to gain adequate exposure to the upper abdomen.
The stomach should be inspected to assess the location and extent of
tumor. The size and location of the primary tumor dictate the extent of gastric
resection. A D2 lymphadenectomy sparing the spleen and pancreas can be done
safely and provides an excellent specimen for surgical and pathologic staging, but
this procedure should only be performed by or with an experienced surgeon.

The D2 subtotal gastrectomy commences with mobilization of the greater

omentum from the transverse colon. After the omentum is mobilized, the anterior
peritoneal leaf of the transverse mesocolon is incised along the lower border of the
colon, and a plane is developed down to the head of the pancreas. The infrapyloric
lymph nodes are dissected and the origin of the right gastroepiploic artery and vein
are ligated.

With a combination of blunt and sharp dissection, the plane of dissection

continues on to the anterior surface of the pancreas, extending to the level of the

49

common hepatic and splenic arteries. This maneuver can be tedious, but
theoretically it provides additional protection against serosal spread of tumor to
the local peritoneal surface.

The right gastric artery is ligated. At this point, the duodenum is divided
distal to the pylorus. The stomach and omentum are then reflected cephalad. The
gastro hepatic ligament is divided close to the liver up to the gastro esophageal
junction. Dissection is then continued on the hepatic artery toward the celiac axis.
Once near the celiac axis, the lymph node bearing tissue is dissected until
the left gastric artery is visualized and can be divided at its origin.

The proximal peritoneal attachments of the stomach and distal esophagus

can then be incised, and the proximal extent of resection is chosen. For tumors of
the mid- and proximal stomach, dissection of the lymph nodes along the splenic
artery and splenic hilum is important.

This technique is not indicated for antral tumors, given the low rate of
splenic hilar nodal metastases seen with these tumors. The stomach is then divided
5 cm proximal to the tumor, which dictates the extent of gastric resection.

Despite the fact that the entire blood supply of the stomach has been
interrupted, a cuff of proximal stomach invariably shows good vascularization
from the feeding distal esophageal arcade.

50

When feasible, most surgeons prefer to anastomose jejunum to stomach

versus esophagus because of the technical ease and excellent healing.
Reconstruction using a variety of techniques has been described and is a matter of
personal choice.

TREATMENT OF ADVANCED DISEASE (STAGE IV)

Chemotherapy versus Best Supportive Care
Patients receiving chemotherapy as part of their treatment have a better
overall survival than those receiving best supportive care only, with an overall
hazard ratio of 0.39 (95% CI, 0.28 to 0.52). The median survival was improved
from 4.3 months for best supportive care to approximately 11 months for
chemotherapy.

Single-Agent Chemotherapy
For most drugs, a variety of doses and schedules have been studied. In the
absence of comparative trials using the same agent with different doses and
schedules, superiority of one regimen over the other cannot be assessed.

Combination Chemotherapy

Like other malignancies, multidrug regimens using agents that have a

single-agent activity have been extensively studied in gastric cancer.

51

One of the most widely used combination chemotherapy regimens in upper

gastrointestinal tract malignancies, including gastric cancer, is the two-drug
combination of cisplatin and fluorouracil.

Other

combination

chemotherapy

regimens

include

methotrexate,

fluorouracil, and doxorubicin (FAMTX); etoposide, leucovorin, and fluorouracil

combination; fluorouracil plus irinotecan; docetaxel added cisplatin fluorouracil;
epirubicin-cisplatin-fluorouracil; irinotecan-fluorouracil-leucovorin ; Cisplatin
Plus Irinotecan; Fluorouracil-Leucovorin-Oxaliplatin (FOLFOX)

Targeted Therapy
Bevacizumab
As with other solid tumors, including colorectal cancer, breast and lung
cancers, therapeutic agents with a specific tumor target are now entering study in
gastric and gastroesophageal junction tumors. One of the first compounds studied
was bevacizumab, a humanized monoclonal antibody that binds the vascular
endothelial growth factor ligand. Bevacizumab can safely be given with cytotoxic
chemotherapy, including in patients in whom the primary tumor was still in place.
Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors
Both erlotinib and gefitinib have been studied in gastroesophageal junction
and gastric cancers. The bulk of the data is currently available only an abstract
form. Cetuximab, an antibody to the epidermal growth factor receptor, is
undergoing study as a single agent and also in combination with systemic
cytotoxic chemotherapy.

52

Radiation for Palliation

To date, no studies have evaluated the use of radiation therapy in patients

with locally recurrent or metastatic carcinoma of the stomach. Its use is likely to
be limited to palliation of symptoms such as bleeding or controlling pain
secondary to local tumor infiltration.
Although minimal data are available, radiation therapy seems to be fairly
effective (from anecdotal experience) in controlling bleeding, as is true in other
sites. This can often be accomplished at relatively low radiation doses. Pain from
local tumor invasion can also be palliated, although the dose required is higher (45
Gy).
Long-Term Side Effects of Therapy
Relatively little has been written in the oncology literature on the local
effects of therapy for gastric cancer and its long-term implications. The presence
of dumping syndrome is well known, with its resulting diarrhea and cramping, but
vasomotor effects such as palpitations and diarrhea also occur either very shortly
after a meal or 1 to 3 hours later. These symptoms probably result from rapid
transit of food from the stomach into the small bowel with the release of various
gastrointestinal hormones. These symptoms can be managed by adjusting the
volume of oral intake and other dietary manipulations. There is also a reactive
hypoglycemia that can result from the rapid insulin release after a meal with little
gastric reservoir.In addition to dumping, there are a number of malabsorption
issues that can be important. B12 malabsorption is well known, and many patients
are placed on monthly supplements, even if it is not clearly needed.

53

After partial gastrectomy one can often monitor B12 levels and replace
when needed. Iron and calcium absorption is improved by the gastric acid that is
eliminated or decreased by surgery or radiation therapy, and bypassing the
duodenum also decreases absorption. Low iron is discovered when patients
develop an iron deficient anemia, but calcium malabsorption may not be found for
many years when the patient develops osteopenia. Patients should be followed
with dual energy x-ray absorptiometry scans and/or placed on calcium
supplementation (calcium citrate is better absorbed than calcium carbonate).

54

METHODOLOGY

The present study was undertaken at K.R. Hospital , Mysore from the period
January 2009 to July 2010 and included patients presenting to the out and in
patient departments at K.R.Hospital, Mysore. The tissue for diagnosis was
obtained by endoscopy or following surgical resection.
Source of Data
Patients presenting to K.R. Hospital, Mysore during the study period and those
found eligible were included in the study.
Sample size: Minimum of twenty five cases meeting criteria of the present study
Inclusion Criteria
Only patients with histological proven carcinoma stomach were included
Exclusion criteria
Patients with tumour recurrence
Investigations
Routine Blood investigations like Haemoglobin%, Total Count, Differential
Count, Bleeding Time, Clotting time.
Renal parameters like Blood Urea and Serum Creatinine
Liver Function Tests
Serum Electrolytes
Chest X-Ray
Blood Grouping
Special investigations like Upper Gastointestinal Endoscopy, USG Abdomen and
CT Scan Abdomen

55

The cases were studied with importance given to clinical history regarding nature
of presentation including diet history. The study of association of risk factors was
also undertaken. Thorough clinical examination, Ultrasonography, endoscopy, CT
in few cases and histopathologic diagnosis formed the basis of the study.
The anatomic site of occurrence, the macroscopic type and the histopathologic
type were studied in each case.
An earnest attempt was made to study all the cases in detail with serial follow-up,
the latter being incomplete due to non-responsive patients.

56

RESULTS

58

RESULTS
ANNUAL PREVALENCE: Graph-1

Gastric carcinoma is a common cancer with almost evenly distributed

annual prevalence.
The number of cases reported was greater in the first half of the year.

No. of cases

Graph-1
Annual distribution of cases from 2009 to July 2010
8
6
4
2
0

2010
2009
Jan Feb Mar Apr May Jun Jul Aug Sep Oct Nov Dec

59

SEX PREVALENCE: Table 7; Graph 2

Gastric cancer is more common in males with 75% of the cases being
males in this study. The Male: Female ratio was 3:1.

Table-7. Sex distribution among carcinoma stomach patients

Present study
Sex
Cases

Male

24

75

Female

25

60

AGE PREVALENCE: Table 8; Graph 3

Carcinoma stomach is more common in the older age group with

increasing incidence after the age forty five. The maximum number of cases was
seen between the age groups 45 to 65. The youngest patient was aged 33 and the
oldest 79.

Table-8. Age distribution among carcinoma stomach patients

Present study
Total
%
0
1
5
9
9
6
2

Age
<25
25-34
35-44
45-54
55-64
65-74
75+

M
0
3.12
15.6
28.1
28.1
18.75
6.25

0
1
3
6
7
6
1

F
2
3
2
1

Graph 3- Age distribution in carcinoma s tomach patients

8
7
6
5
4
3
2
1
0

Male
Female

<25

25-34

35-44

45-54

61

55-64

65-74

75+

SOCIOECONOMIC STATUS: Table 9; Graph 4

In the present study majority of the patients(75%) belonged to the low

socioeconomic status. The prevalence among the high socioeconomic group could
not be studied as none of the patients belonged to this strata.

Table 9- Income group among carcinoma stomach patients

Income Group

Present study
Cases

Low

28

87.5

Middle

12.5

High

62

RISK FACTORS: Table 10; Graph 5.0, 5.1

There are strong suggestions of the influence of environmental factors on

gastric cancer. The most common risk factors associated were spicy food and
mixed diet followed by tobacco and alcohol use.

In this study twenty seven(84.4%) patients consumed mixed diet and the
rest were vegetarians. The non vegetarians took meat/fish approx. thrice every
week.

All patients in the study group frequently and regularly consumed green
leafy vegetables.

Fruit consumption was frequent only in twenty two(68.7%) of the cases

with predominant of them being males(86.4%). Only three(13.6%) of the females
frequently consumed fruits.

High salt intake was not reported by any of the subjects in this study
although this value was not quantified and hence significance could not be
ascertained.

63

Smoked foods though a common risk factor in many countries was

consumed only by Five (15.6%) of the patients and even in theses patients the
intake was not frequent. Majority of the patients, twenty seven(84.4%) reported to
the use of high spicy diet in everyday food.

Tobacco smoking in the form of cigarette and beedi smoking was seen in
nineteen (59.3%) patients, all being males. Five females and three males reported
to frequent use of betelnut which has been shown to a risk factor in the
development of gastric cancer.

Alcohol consumption was seen in sixteen(50%) of the patients, all males,

who consumed it regularly and for a period of more than ten years.

Table 10 - Comparision of risk factors between males and females, F- Frequent,

O-Occasional
Risk factor
Mixed diet
Veg diet
Green leafy
Fruits
High salt intake
Smoked Foods
Spicy
Smoking
Alcohol
Betel nut

F
O
F
O

Total
Cases
27
5
32
0
22
10
0
5
27
19
16
8

%
84.4
15.6
100
68.7
31.3
15.6
84.4
59.3
50
25
64

Males(24)
Cases
%
20
74.1
4
80
24
75
0
19
86.4
5
50
4
80
21
77.7
19
100
16
100
3
37.5

Females(8)
Cases
%
7
25.9
1
20
8
25
0
3
13.6
5
50
1
20
6
22.2
5
62.5

65

BLOOD GROUP: Table 11; Graph 6

Blood group A showed the highest association with gastric cancer patients
with fourteen(43.7%) cases followed by blood group O and B.

Table 11 - Blood group distribution in carcinoma stomach patients

Study
Present Study

A+
14(43.7)

66

Blood Group (%)

B+
AB+
5(15.6)
1(3.1)

O+
12(37.5)

SYMPTOMS: Table 12, Graph 7

Anorexia was the most common symptom in patients and was reported in
twenty six (81.25%) of the patients. The next most common symptom was nausea
and vomiting reflecting the high prevalence of distal tumours. Twenty three
(71.8%) reported weight >10% of body weight.

Proximal tumours involving the gastooesophageal junction had dysphagia

as the predominant symptom. Only one patient in this study presented with
jaundice and none of the patients had supraclavicular lymphadenopathy at
presentation. One patient presented with features of peritonitis and was found to
have a growth in the body of the stomach which had perforated.

Early satiety was reported in sixteen (50%) of the patients which is

characteristic of tumours involving the stomach wall diffusely.

Symptom analysis among the two sexes revealed that nausea, vomiting and
weight loss were the most common symptoms followed by pain abdomen in
females. The most common symptoms in males were anorexia, abdominal pain
followed by nausea and vomiting.

67

Table 12-Symptom analysis in patients of carcinoma stomach

Present study
Cases
%

Males n=24
Cases
%

Females n=8
Cases
%

Abdominal Pain

22

68.75

16

66.6

75

Nausea/vomiting

24

75

19

79.2

62.5

Weight loss

23

71.8

15

62.5

100

Anorexia

26

81.25

18

75

100

Early satiety

16

50

12

50

50

Jaundice

3.2

4.2

Dysphagia

15.6

16.6

12.5

Malaena

21.8

20.8

24

Others

6.25

4.4

12.5

Symptoms

68

SIGNS: Table 13, Graph 8

Overall, anemia was the most common sign in twenty one (65.6%) of the
cases followed by dehydration and ascites.

Visible gastric peristalsis the characteristic sign of gastric cancer was seen
only in four (12.5%) of the cases. Gastric cancer presented as mass abdomen in
six (18.75%) cases.

In females, anemia and ascites were the most common symptoms. None of
the females in this study had visible gastric peristalsis which was seen in three
(12.5%) of males.

Presentation with mass abdomen was commoner in females (37.5%) than

in males (12.5%).

Ascites at presentation suggesting the advanced stage of the disease was

more common in females (50%) compared to males (31.25%).

69

Table 13 - Analysis of signs in gastric cancer patients

Signs

Total
cases

Male n=24

Female n=8

Cases

Cases

Anemia

21

65.6

14

58.3

87.5

Icterus

3.12

4.2

Dehydration

10

31.25

29.2

37.5

Ascites

10

31.25

25

50

VGP
Mass abdomen

4
6

12.5
18.75

4
3

16.6
12.5

37.5

70

SUBSITES: Table 14; Graph 9

The antrum was the most common site of affliction accounting for 75% of
all subsites. This was also similar in both the sexes with percentages of 70.8 in
males and 87.5 in females. Oesophagogastric tumours accounted for 9.37% of the
cases and were similar in both the sexes. None of the females in this study had
cancers of the body and proximal stomach.

Table 14- Sub site specific trends in carcinoma stomach

Sub site

Total

Male

Oesophagogastric jn

Cases
3

%
9.37

Cases
2

%
8.3

Cases
1

%
12.5

Proximal stomach

6.25

8.

Body

9.37

12.5

Antrum

24

75

17

70.83

87.5

71

Female

MACROSCOPY: Table 15

The predominant macroscopic subtype was Borrmann type II with eleven

(34.5%) followed by types III and IV. In males the predominant type was
Borrmann type II (41.6%) where as in females it was type IV(62.5%). Females
had a higher percentage of locally advanced lesions. There were no Bormann type
I lesion in females in this study.

Table 15- Comparison of the macroscopic type in both sexes

Borrmann Type

Total

Male

Female

Cases
5

%
15.6

Cases
5

%
20.8

Cases
0

%
-

II

11

34.4

10

41.66

12.5

III

25

25

25

IV

25

1.5

62.5

SITE AND SYMPTOMS: Table 16; Graph 10

Antral lesions presented predominantly with nausea/vomiting, weight loss,

anorexia and pain abdomen. 50% of the antral growth patients also reported early
satiety.

72

Oesophagogastric tumours had dysphagia as the predominant symptom

along with weight loss and anorexia reflecting the aggressive nature of such
tumours. Similarly these entire lesions also had dysphagia as a symptom. Malena
was more common in lesion of the body followed by the antrum.

Table 16 - Comparision of symptoms with the site of the tumour

Symptoms

Total
cases

Site of Tumour

Abdominal Pain

22

Antrum (24)
Cases %
15
68.2

Nausea/vomiting

24

21

87.5

50

33.3

33.3

Weight loss

23

17

70.8

100

33.3

100

Anorexia

26

21

87.5

100

100

Early satiety

16

12

50

50

66.6

33.3

Jaundice

4.2

Dysphagia

100

100

Malaena

8.33

50

100

Others

4.2

33.3

73

Proximal (2)
Cases %
2
100

Body (3)
Cases %
3
100

OGJ (3)
Cases %
1
33.3

MACROSCOPY AND SYMPTOMS: Table 17; Graph 11

Borrmann type I lesion patients experienced pain abdomen and vomiting in

almost 80% of cases. All Borrmann type II lesion patients had symptoms of
nausea/vomiting, weight loss and anorexia. Type II and III lesion patients had
early satiety in 72.7% and 50% respectively.

Table 17- Comparision of symptoms with macroscopic appearance

Symptoms

Abdominal Pain
Nausea/vomiting
Weight loss
Anorexia
Early satiety
Jaundice
Dysphagia
Malaena
Others

Total
cases
22
24
23
26
16
1
5
7
2

I n=5
Cases
4
4
3
2
-

%
80
80
60
40
-

Borrmann type
II n=11
III n=8
Cases %
Cases
9
81.8 5
11
100 6
11
100 6
11
100 6
8
72.7 4
3
1
1
9.1
3
2

74

%
62.5
75
75
75
50
60
12.5
37.5
25

IV n=8
Cases
4
3
5
5
2
4
3
-

%
50
60
62.5
62.5
25
50
37.5
-

SITE AND SIGNS: Table 18, Graph 12

All cases of proximal tumours had anaemia at presentation. Tumours of the

body(66.6 %) had ascites at the time of presentation. All the cases with visible
gastric peristalsis were antral growths, however only 16.6% of antral growths had
visible peristalsis.
Table 18 - Analysis of the site of tumour with signs
Signs

Anaemia
Icterus
Dehydration
Ascites
VGP
Mass abdomen

Total
cases
21
1
10
10
4
6

Antrum (24)
Cases %
14
58.3
1
4.2
6
25
5
20.8
4
16.6
5
20.8

75

Site of Tumour
Proximal(2)
Body(3)
Cases %
Cases
2
100
2
1
50
2
1
50
2
1

%
66.6
66.6
66.6
33.3

OGJ(3)
Cases
3
1
2
-

%
100
33.3
66.6
-

MACROSCOPY AND SIGNS: Table 19; Graph 13

Majority of type II (81.8%) and type III (87.5%) lesions presented with
anemia. Borrmann type II, III and IV lesions were more often associated with
ascites than type I lesions. Type II and Type III lesions accounted for the majority
of cases of mass abdomen.
Table 19 - Comparison of macroscopy with clinical signs
Signs

Anaemia
Icterus
Dehydration
Ascites
VGP
Mass abdomen

Total
cases
21
1
10
10
4
6

I (5)
Cases
1
-

Borrmann
II (11)
III(8)
Cases %
Cases
9
81.8 7
1
5
45.5 3
4
36.4 3
3
27.3 1
3
27.3 2

%
25
-

76

%
87.5
12.5
37.5
37.5
12.5
25

IV(8)
Cases
4
2
3
1

%
50
25
37.5
12.5

HISTOPATHOLOGY: Table 20, Table 21

Majority of the cases were well differentiated adenocarcinoma with 62.5% of the
cases. Females had a higher percentage of poorly differentiated tumours.
Table 20- Comparison of histopathology
Histology

Present study

Differentiation

Total

Male

Female

Well

18

56.25

13

54.2

62.5

Moderately

21.87

29.2

25

Poorly

21.87

29.2

37.5

Undifferentiated

Antral tumours were predominantly well differentiated and oesophageal had high

percentage of poorly differentiated tumours.

Table 21- Comparision of histology with the site of the tumour

Histology

Present study

Differentiation

Total

Antrum

Body

Proximal

OEJ

Well

18

11

Moderately

Poorly

Undifferentiated

77

DISCUSSION

78

DISCUSSION
There have been widespread reductions in gastric cancer incidence and mortality
around the world in the last 50 years, which have been described by some authorities
as an unplanned triumph. Nonetheless, gastric cancer is still estimated to account
for about 10% of invasive cancers worldwide and is the second leading cause of
cancer death. The incidence of gastric cancer varies greatly across populations.
This study was undertaken to study the prevalence of gastric cancer as occurring in
K.R. Hospital, Mysore which is a tertiary care centre with a large input of cases from
Mysore and its surrounding districts.
The study had certain drawbacks. The association of H. Pylori with gastric carcinoma
was not studied. Since histopathological confirmation was an inclusion criteria for the
study, many suspected cases were not included for lack of definite tissue diagnosis.
Although CT abdomen is recommended for the staging of the disease, it was not
performed in most of the cases due to financial constraints. Many cases were referred
to the regional cancer institute for further treatment.

Gastric cancer is more common in males with the global age-standardized incidence
for males about 2.2 times higher than for females circa 199029.30,31. Males had
higher rates in all regions. Men have greater exposure to one or more environmental
carcinogens and are more susceptible29. Similar observations were made in this study
with M:F ratio of 3:1. These observations are comparable to similar studies in India.
79

Table 21. Sex distribution among carcinoma stomach patients

Sex
Male
Female

Gajalakshmi et al 199532

Sumathi et al 200919

Present study

Cases
287
101

Cases
64
25

Cases
24
8

%
73.9
26.1

%
71.9
26.9

%
75
25

Age wise trends in carcinoma stomach have been reported worldwide being largely a
disease of the older age groups in most countries. In this study maximum no of cases
was seen after the age of 45 years. Urmi Sen et al33 studying cancer patterns in
eastern India also noted a similar age trend with increasing incidence of gastric cancer
with age. In this study the youngest patient was aged thirty three and the oldest
seventy nine.

Table 22. Age distribution among carcinoma stomach patients

Age

<25
25-34
35-44
45-54
55-64
65-74
75+

Gajalakshmi C K et al
1996
Cases
%
2
0.5
30
7.7
64
16.5
84
21.6
124
32.0
68
17.5
16
4.1

Sen et al 200233

Present study

Cases
0
7
1
20
53
77
120

Cases
0
1
5
9
9
6
2

%
0.1
0.5
2.2
7.2
19.2
28.0
43.4

80

%
0
3.12
15.6
28.1
28.1
18.75
6.25

As the study was conducted in a Government Hospital majority of the cases belonged
to the low socioeconomic status accounting for 75% of the cases. The scenario is
similar across India where majority of the population belong to the low
socioeconomic group further contributing evidence of dietary role of carcinogens.
Studies at Chennai and other parts of the country have shown consistent correlation
between the lower socioeconomic group and higher prevalence of gastric cancer.
Table 23- Socioeconomic groups among gastric cancer patients

Sex
Male
Female

Gajalakshmi et al
1995
Cases
%
287
73.9
101
26.1

Sumathi et al
2009
Cases
%
64
71.9
25
26.9

Present study
Cases
24
8

%
75
25

The association of blood group A is well known and the findings were compared with
other studies

Table 24: Blood group distribution in carcinoma stomach patients

Study
Kamlesh Guleria et al., Punjab34
Jose et al, Kerala35
Present Study

A+
01 (12.5)
26(37.1)
14(43.7)

Blood Group (%)

B+
AB+
05 (62.5)
14(20)
07(10)
5(15.6)
1(3.1)

O+
02 (25.0)
23(32.85)
12(37.5)

Gastric cancer is known to be associated with several environmental risk factors of

which diet has an important role. The association of diet has been studied in many
studies and consistent results obtained all over. The findings of this study were
compared with Sumathi et al. Majority of the patients were non vegetarians in both
the studies.
81

The association of tobacco use and alcohol has been studied. In this study
nineteen(59.35%) of the patients reported to the use of smoking for a significant
periodic compared to 40.5 patients in study by Sumathi et al. Betelnut chewing seen
more in females was seen in 25% of the patients compared to 10.2% in the other
study.

Table 25- Comparision of risk factors between males and females, F- Frequent, OOccasional
Factor
Mixed Diet
Veg Diet
Green leafy veg
Fruits
High Salt intake
Smoked foods
Spicy food
Smoking
Alcohol
Betelnut

Sumathi et al n=89
Total
%
89
100
0
F 58
65.2
O 31
34.8
F 39
43.8

Present study n=32

Male Female Total
20
7
27
4
1
5
24
8
32
19
3
22

%
84.4
15.6
100
68.7

5
4
21
19
16
3

31,3
15.6
84.4
59.3
50
25

50
36
32
9

56.2
40.5
35.9
10.2

5
1
6
5

10
5
27
19
16
8

Abdominal pain was major symptom reported in twenty two(68.75%) of the cases
compared to 56.6% in a study by Safaee et al. Weight loss was seen in twenty
three(71.8%) of cases compared to 57.7 cases. These findings suggest that patients in
our set up present in an early stage of the disease with both local and regional spread.
The percentage of patients presenting with malaena was comparable in both groups.

82

Table 26 Symptom analysis in patients of carcinoma stomach

Symptoms
Abdominal Pain
Nausea/vomiting
Weight loss
Anorexia
Early satiety
Jaundice
Dysphagia
Malaena
Others

Safaee et al36
2009
Cases %
425
56.6
324
43.2
434
57.7
263
31.5
263
31.5
144
19.1
-

Present study
Cases
22
24
23
26
16
1
5
7
2

%
68.75
75
71.8
81.25
50
3.2
15.6
21.8
6.25

The west has noted a paradigm shift in site of gastric cancer tumours with a steady
increase in tumours of the cardium and proximal tumours and a decline in distal
tumours.
In this study distal tumours continued to be the most common site of affliction with
24(75%) cases and only 5 cases(15.6%) of proximal tumours. Cherian et al8 studying
a 16 year trend of gastric cancer at Chennai also had similar findings.

83

Table 27 Sub site specific trends in carcinoma stomach

Sub site
Oesophagogastric jn
Proximal stomach
Body
Antrum

Cherian et al8
Cases
%
65
3.78
97
5.64
400
23.27
1157
67.31

Present study
Cases
3
2
3
24

%
9.37
6.25
9.37
75

In this study majority of the tumours were well differentiated. Moderately and poorly
differentiated were equally differentiated. In the study by Safee et al poorly
differentiated tumours were more common..

Table 28 Comparision of histology according to Broders classification

Histology
Safaee et al36
Present study
Differentiation
Cases
%
Cases
Well
113
23
18
Moderately
142
30.1
7
Poorly
203
43
7
Undifferentiated 14
3
-

84

%
56.25
21.875
21.875
-

CONCLUSION
The incidence of gastric cancer varies greatly across populations. In many parts of the
world, however, the incidence of gastric cancer has gradually decreased, principally
because of changes in diet, food preparation, and other environmental factors.

This study was undertaken to study the prevalence of gastric cancer as occurring in
K.R. Hospital, Mysore which is a tertiary care centre with a large input of cases from
Mysore and its surrounding districts.

Gastric cancer is more common in males with the global age-standardized incidence
of gastric cancer for males was about 2.2 times higher than for females circa 1990.
Males had higher rates in all regions. Similarly in this study gastric cancer was more
prevalent in males with a sex ratio of 3:1.

Majority of the patients belonged to the lower socioeconomic strata and had
association of risk factors. Blood group A was the prevalent blood group.

The disease was more prevalent in patients above the age of 45 with the oldest being
seventy nine. Majority presented in the advanced stage of the disease although there
were few cases which presented in the early gastric carcinoma stage.

85

The pylorus remained the most common site of affliction in contrast to western
countries which have showed a consistent shift towards proximal tumours. The major
percentage of the tumours was well differentiated.

The findings of this study are comparable to other similar studies in India and
proximal gastric tumours continue to be the major subtype in this part of the world
and association of risk factors increase the likelihood of an individual developing
gastric cancer.

Preventive strategies offer the best opportunities for control of the disease, for several
reasons. Prevention intervention trials involving antioxidant supplements and anti-H.
pylori treatment have shown beneficial effects in preventing the progression of
pathologic changes in the gastric mucosa.
On the other hand, recent advances related to differences in the genotypes of the
bacteria and in human cytokine polymorphisms would allow the design and
implementation of large-scale screening programs to identify subjects at the highest
risk of gastric cancer.

86

SUMMARY
Gastric cancer continues to be a disease of the older age group with increasing
prevalence after the age of forty five suggesting the role of environmental
carcinogens.

Males are affected more predominantly than females and the lower socioeconomic
strata of the society are more commonly involved.

Patients usually present in the advanced stage, however with the increasing use of
upper gastrointestinal endoscopy early gastric cancers are also being detected.

The association of risk factors is well known and consistent and hint at the primordial
prevention of the disease.

Distal tumours continue to be the major subtype in this study.

Successful preventive strategies have to be developed a multidisciplinary approach

should combine population screening with molecular biological techniques that are
being developed.
87

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93

ANNEXURES

94

A CLINICO PATHOLOGICAL STUDY OF GASTRIC CARCINOMA

PROFORMA
Case No:
Name:
Occupation:
Address:
Socioeconomic Status:

Age:

DOA:
Result : Relieved/Died
Final Diagnosis:

DOS:

Symptoms:
a. Abdominal Pain:
c. Weight loss:
e. Early satiety:
g. Dysphagia:
i. Other symptoms:

DOD:

b. Nausea/vomiting:
d. Anorexia:
f. Jaundice
h. Malaena:

Past History: Prior gastric surgery

Gastric atrophy/Gastritis
Family History:
Diet History:Vegetarian/Non-Vegetarian
Animal proteins:
Complex carbohydrates:
Green leafy vegetables and fruits:
High Salt intake:
Smoked foods:
Spices
Tobacco use/Pan chewing:
Alcohol:
Use of ground water:
GPE:
Built:
Pallor:
Vitals: BP-

Nourishment:
Icterus:
PR-

Sex:
IP No:

Hydration:
Lymphadenopathy:

RR-

Temp-

Systemic Examination:
P/A:
Inspection:
a. Distension/fullness
b. Dilatedd veins
c. Visible mass
d. Visible gastric peristalsis
e. Umbilicus
f. Movements of abdominal quadrants

95

Palpation:
Mass
a. Site
b. Size
c. Shape
d. Surface
e. Borders
f. Consistency
g. Moblility
h. Movement with respiration
i. Succussion splash
j. Organomegaly
k. Left supraclavicular node
Percussion:
Over the mass
Liver span
Shifting dullness
Auscultation:
P/R:
Other Systemic Examination;
R/S:
CVS:
CNS:
Investigations
Routine: HaemoglobinTotal CountCTBTBlood Urea:
Serum Creatinine:
Random Blood Sugar:
Liver function tests:
Serum Electrolytes:
Blood Group:
Chest X-Ray:

ESRDifferential Count-

Special Investigations:
Upper GI Endoscopy:
USG Abdomen:
CT Scan Abdomen:
Biopsy:
Treatment:
Surgery:
Operative procedure:
Findings:
Post operative period:

96

Examination of the specimen:

Site of growth: Pylorus/Antrum/Body/Fundus/cardiooesophageal junction
Type of growth: Polypoidal/Fungating
Ulcerative with elevated/depressed edges
Diffuse/Infiltrative
Unclassifiable
Histopathology:
Chemotherapy:
Follow up:

97

Fig. 7 Endoscopic photograph showing ulceroproliferative growth

in antrum

Fig.8 Endoscopic photograph showing early gastric cancer

98

Fig. 9 Photograph showing gastric cancer invading the posterior wall and
perforating it

Fig. 10 Photograph showing palliative anterior gastrojejunostomy

99

Fig. 11 Photograph showing partial gastrectomy specimen

Fig. 12 Photograph showing opened partial gastrectomy specimen

100

5331

Virajpet, Kodagu

19/03/09 07/04/09 23/04/09

OP41283 Kukkeri,K.R. Pet

9.8 A +

Chemo

HPR

60

Findings

65

8 Babu Ray

Treatment

7 Sannaswamy

CT

Age

4073

USG

UGI

12/03/09

60

Macro

6 Sivamma

Blood gr

04/03/09

2105

Hb

Kenchamalipura,H.D.Kote

1345

PR

08/02/09

45

Mo

Mass

29/01/09

Nagahalli,K.R.Pet

72

5 Krishne Gowda

Ascites

Ayarhalli, Mysore

4 Nanjappa

VGP

BPL NS

b,c

lymphaden

a,c,d

Jaundice

31/01/09

OP21370 Nelavagilu,Hunsur

Anaemia

28/01/09

Hydration

24/01/09

54

Alcohol

Fruits

Ramnathpura, Hasan

50

3 Muddaiah

Betelnut

Veg

873

2 Thimamma

Tobacco

Spices

Salt

Smoked F

Diet

Past His

60

Name

SE status

BPL NS M

DOD

21/01/09 26/01/09 10/02/09 a,b,c,d,e

DOS

ChokanaHalli, K.R. Pet

DOA

IP no
587

Place

Sex
M

1 Somashekar

No

Symptoms

MASTER CHART

PA,U

PG,GJ

PA,G,PGLN, MA

WD

Mo

8.6 O +

U,PA

SWT,A

WD

BPL NS M

Mo

10 O +

PA,U

NS

WD

16/02/09 a,b,c,d,e,h BPL NS M

Mo

6.8 A +

PA, I,PO

SWT

MD

12/02/09

BPL NS M

Mo

14 O +

PA,Po,G

NS

WD

a,b,c,d,e,h,i BPL NS M

Mo

B+

PA,I

SWT,MA

b,e

a,c,d,g,h BPL NS

Mo

A+

I,C,F,GEJ

MA

a,b,c,d,f

APL NS M

Mo

10 O +

PA,GOO,I

DS,A, MRD

BPL NS M

Mo

10 O +

PA,I,GC

SWT,PGLN

BPL NS

Mo

14 AB + 2

PA,U,LC

SWT,MA

b,c,d,e

BPL NS M

Mo

A+

PA,U

SWT

a,b,d

A+

PA,Po,G

NS

6.6 O +

I, F,GC,GEJ

SWT,LS,A

9 Subbe Gowda

50

6413

Kanchinakere,K.R.Nagar

03/04/09 08/04/09 21/04/09

b,e

10 Somachary

60

6783

Mahadevapura,SR Patna

11/04/09 16/04/09 27/04/09

a,b,c

11 Mahapeez

61

6987

Mandi Mohalla,Mysore

17/4/09

12 Marigowda

60

8642

DhoddaKoppalu, Pandpur

03/05/09

18/05/09

BPL NS M

Mo

13 Syed Ahmed

50

8995

Kesare,Mysore

07/05/09

25/05/09 a,b,c,d,g,h BPL NS M

Mo

14 Siddappa

27/04/09 12/05/09

WD
-

MD

PG, GJ

PA G, PGLN,A

MD

PG,GJ

PA,G,PGLN, MA

PD

PGJ

IO,PALN,A

PD

PG,GJ

O,PGLN,MA

PD

EGC

WD

5 FU

53

10351

Hullanehalli,Chamrajnagar

22/05/09

30/05/09

a,b,c,d

BPL NS M

Mo

10 A +

PA,I,PO

NS

MD

15 Narayan Swamy 61

10533

Gandhi Nagar,Mysore

24/05/09

25/05/09

c,d,e,g

APL NS

Mo

10 O +

GEJ,I,DC

WD

16 Puttamadaiah

51

26/05/09

a,b,d

APL NS M

Mo

13 A +

PA,Po,G

17 Thimmegowda

40

11486

H.Matakere,H.D.Kote

03/06/09 08/06/09 17/06/09

a,b,d

BPL NS M

Mo

12 B +

UG,PA,PO

SWT

18 Ravi

33

12276

Kailashpuram,Mysore

11/06/09 27/06/09 13/07/09

b,c,d,e

BPL NS M

Mo

11 A +

U.PA.PO

MRD

19 Nanjappa

65

12305

Siddnapura,Gundulpet

25/06/09 30/06/09 13/07/09

a,d,e

BPL NS M

Mo

O+

UG,PA

MA

20 Bheemaiah

60

17528

Hosapura,Nanjungud

11/08/09 18/08/09 28/08/09

b,c,d,e,

BPL NS M

Mo

10 A +

U,PA

SWT,MA

21 M G Nanjunda

74

20233

SuntiKopppa,Kodagu

31/08/09

13/09/09

a,e,h

Mo

7.4 O +

U,GC

22 Annamalay

67

21831

Somvarpet, Kodagu

08/09/09

18/09/09

a,e

BPL NS M

Mo

11 A +

Po,GC

23 Sannaiah

65

27584

Nargonahalli,K.R.Pet

16/11/09 16/11/09 13/12/09 a,b,c,d,e,h,i BPL NS M

Mo

6.4 O +

24 Javare Gowda

79

1294

Dadadalli, Mysore

06/02/10 09/02/10 08/03/10

a,b,c,d

BPL NS M

Mo

11 0 +

25 Puttamma

75

3767

Arkalavadi,Chamrajnagar

22/02/10 26/02/10 10/03/10

a,c,d

BPL NS M

Mo

26 Gowramma

35

5021

ChuchunakatteHobli,K.R.N 27/02/10 02/03/10 11/03/10

b,c,d,e,

BPL NS M

Mo

10 B +

27 Mallikarjuna

40

5425

Yarigur, Yalundur

c,d,g

BPL NS M

Mo

A+

28 Shoba

40

5443

Kuvempu Nagar, Mysore

04/03/10

13/03/10 a,b,c,d,g,h APL NS M

Mo

29 Shanthimallappa 53

7717

VijayNagar, Mysore

29/03/10 09/04/10 24/04/10

b,c,d,e,

BPL NS M

Mo

14226

HoleNarasipura,Hasan

02/06/10 11/06/10 18/06/10

a,b,c,d

BPL NS M

Mo

10 O +

a,b,d

BPL NS M

Mo

12 A +

BPL NS M

Mo

10 B +

4 G,PA,GC,LC,B SWT,PALN,A

OP90350 Kuvempu Nagar,Mysore

30 Laxmamma

50

31 Chikkegowda

57

M OP141326 Herikyathanahalli,Hunsur

32 Rachamma

50

20171

Hullahalli, Nanjungud

04/03/10 12/03/10 20/03/10

18/07/10

30/07/2010 10/08/10 01/09/10 a,b,c,d,e

BPL NS

WD

IO,I,PA,PALN,PHLN

WD

PG,GJ,FJ

O,G PA, PGLN

WD

WD

PG,GJ

O.PG,PGLN

MD

5 FU

SWT,MA

WD

WD

EL

Per,G,B,A.PAGN

PD

UG,PA,PO

PGJ

IO,PA G,PAGN,A

PD

UG,PA

SWT.A

PGJ

IO,PA G,PAGN,A

WD

PA,U

OC Rt

PG, GJ

O,G, PA

MD

GEJ,I,

MA

FJ

IO, A,PALN

WD

5-FU

B+

GEJ,IG,F,B

SWT,PGLN,A,S

PD

A+

U,PA.PO

SWT

PG,GJ

O,PA G,PGLN,A

MD

UG,PA

SWT

IO,LS,A

WD

PA,Po,G

NS

WD

IO,PA,GC,LC,B,PALN

PD

5-FU

SWT,DC PGJ,JJ
-

KEY TO MASTER CHART

APL- Above Poverty Line

I- Infiltrative

BPL- Below poverty Line

IO- Inoperable

NS- Nothing Significant

JJ- Jejunojejunostomy

M- Mixed

LC- Lesser curvature

V- Vegetarian

LS- Liver secondaries

F- Frequent

MA - Minimal Ascites

O- Occasional

MRD- Medical Renal Disease

Mo- Moderate
O- Operable
A- Ascites
D- Dehydration
B- Body

P- Poor
PA- Pyloric Antrum

C- Cardia
D- Diffuse
DC- Decreased capacity
DS- Dilated Stomach

PALN- Paraaortic Lymph nodes

PE- Pleural effusion
Per- Perforation

EL- Emergency Laparotomy

F- Fundus
FJ- Feeding Jejunostomy
G- Growth
GEJ- Gastro-oesophageal junction
GC- Greater curvature

Po- Polypoidal
PO- Pyloric Obstruction