Stomach Neoplasms
Professor Ravi Kant
FRCS (England), FRCS (Ireland),
FRCS(Edinburgh), FRCS(Glasgow), MS, DNB,
FAMS, FACS, FICS,
Professor of Surgery
Stomach Neoplasm
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Maltoma
Lymphoma
GIST
CA stomach
Gastric Lymphoma
Most common primary GI Lymphoma .
It’s increasing in frequency.
Presentation:
Similar to gastric carcinoma.
May reveal peripheral adenopathy, abdominal
mass or splenomegaly.
Diagnosis:
1.EGD
2.contrast GI x-ray.
3.CT guided fine needle biopsy.
Treatment :
Gastric Lymphoma Rx is
Surgery
(Other organs- preferred Rx of
Lymphoma is Chemotherapy or
Radiotherapy)
Maltoma
Mucosa associated lymphoid
tumour
MALTOMA
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Aetiology= H Pylori
Rx = Rx of H Pylori
= Triple drugs
What are GIST…??
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Gastrointestinal Stromal Tumors are
uncommon mesenchymal tumors that
arise in the wall of the
gastrointestinal tract
It is believed to originate from an
intestinal pacemaker cell called the
interstitial cell of Cajal.
Cajal cell

An intestinal pacemaker cell, has
been proposed the cellular origin of
GISTs. It has characteristics of both
smooth muscle and neural
differentiation on ultrastructural
examination
KIT
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role of the KIT and platelet-derived
growth factor receptor (PDGFR)
tyrosine kinase receptors
KIT receptor tyrosine kinase (KIT RTK)
KIT
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approximately 5% of GIST cells show
not activation and aberrant signaling of
the KIT receptor, but rather mutational
activation of a structurally related
kinase, PDGFR- (PDGFRA).
90% rate of mutations seen in a more
recent series searching for potential
mutations in each of exons 11, 9, 13,
and 17
CD117
GIST
CD34
Actin &
Desmin
S-100
+
-
-
+
Desmoid
tumor
-
+
-
-
True
leiomyosarc
oma
-
-
+
-
Schwanoma -
-
-
+
Diagnosis

CT is the common mode of diagnosis
FDG PET is mandatory
►PET CT scan is ideal
 MR

GIST & chemoresistance


▲ P-glycoprotein [the product of the
multidrug resistance-1 (MDR-1) gene]
▲ MDR protein
Distribution…
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Stomach 50-60%
Small bowel 20-30%
Large bowel 10%
Esophagus 5%
Else where in abdomen 5%
Symptoms…
Abdominal pain
 Dysphagia
 Gastrointestinal bleeding
 Symptoms of bowel obstruction
 Small tumors may be
asymptomatic

Cytologically…
1.
2.

Spindle cell GISTs
Epithelioid cell GISTs
Although GISTs can differentiate
along either or both cell types,
some show NO significant
differentiation at all
Diagnosis…
MUST BE DONE
IMMUNOCHEMICALLY


The CD34 antigen (70-78%)
The CD117 antigen (72-94%)
Malignant Versus Benign
Size
Mitotic count
Very Low risk
<2 cm
<5/50 HPF
Low risk
2-5 cm
<5/50 HPF
Intermediate
risk
<5 cm
5-10 cm
>5 cm
>10 cm
Any size
6-10/50 HPF
<5/50 HPF
>5/50 HPF
Any count
>10/50 HPF
High risk
predictors of survival
significant
Male sex,
on
 Tumor size > 5cm
multivariate
 Incomplete resection analysis

Treatment…

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Surgical excision is primary treatment
option but recurrence rates are high
Resistant to standard chemotherapy
regimens due to over-expression of
efflux pumps
Radiation therapy limited by large
tumor sizes and sensitivity of
adjacent bowel
IMATINIB
 Since activation of Kit played a crucial
role in the pathogenesis of GIST,
inhibition of Kit would be therapeutic

IMATINIB


Orally bioactive tyrosine kinase
inhibitor
Shown to be effective against GIST
tumors in two trials in the US and
Europe reported in 2001 & 2002
Gastrointestinal Stromal Tumor ‘GIST’
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Previously leiomyoma & leiomyosarcoma.
<1 %
Rarely cause bleeding or obstruction.
The origin: Intestinal Cells of Cajal ‘ICC;s’
autonomic nervous system.
The distinction b\w benign & malignant is
unclear. In general terms, the larger the
tumor & greater mitotic activity, the more
likely to metastases.
The stomach is the most common site of
GIST.




Usually are discovered incidentally on
endoscopy or barium meal
The endoscopic biopsies may be
uninformative as the overlying mucosa is
usually normal
Small tumorswedge resection
Larger onesgastrectomy
35
36
GIST
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Case historysubmucosal
Cajal Cell
Gene KIT
PGDRF
Diagnosis
CT
PET
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Rx
Surgery
Chemoresistance
Imatininb
Sumanitib
Prognosis
Predictor factors
37
GASTRIC CARCINOMA
GASTRIC NEOPLASM
Benign
Epithelial
Mesenchymal
Malignant
1.Primary
Adenocarcinoma
Gastrointestinal stromal tumors
‘GIST’
Lymphoma
2. Secondary:
invasion from adjacent tumors.
Gastric Carcinoma
lesion of the stomach.
Epidemiology
Risk Factors
DEFINITION &Malignant
55 year old Japanese male who is living in
Incidence of Gastric Carcinoma:
Japan
& working in industry.
Japan
70 in100,000/year
Europe 40 in 100,000/year
Twice more common
UK 15 in 100,000/year
male than
female
USA 10 in 100,000/year
Japan has the In
world
dustiningestion
occur at anyworldwide.
age
ItCan
is decreasing
highest
Rate of
from a variety
Studies
have
confirmed
But Peak
incidence
gastric cancer.
of industrial
thatyears
incidence
Is 50-70
old. decline in
processes
Japanese
immigrant to
It is more
aggressive
may be a risk.
In younger ages.
America.
Gastric Carcinoma:
Risk Factors
Predisposing :
Environmental:
Genetic:
1. Pernicious anaemia
& atrophic gastritis
(achlorhydra)
2. Previous gastric
resection
3. Chronic peptic ulcer
(give rise to 1%)
4. Smoking.
5. Alcohol.
1.H.pylori infection
Sero(+)patients
have 6-9 folds risk
2.low
socioeconomic
Status
3. nationality
(JAPAN)
4. Diet (prevention)
1.Blood group A
2.HNPCC:
Hereditary nonpolyposis colon
cancer.
Clinical Presentation
Most patients present with advanced stage..
why?
They are often asymptomatic in early stages.
Common clinical Presentation:
The patient complained of loss of appetite that was
epigastric pain
followed by weight loss of 10Kg in 4 weeks.
Bloating
Heearly
hadsatiety
notice
nausea & vomiting*
epigastric
discomfort & postprandial fullness.
dysphagia*
anorexia
He
presented to theDyspepsia
ER complaining of vomiting of
weight quantities
loss
large
of undigested food & epigastric
upper GI bleeding
distension.
(hematemesis, melena,
iron deficiency anemia)
signs
-Anemia.
-Wt. loss ( cachexia)
-Epigastric mass, Hepatomegaly,
Ascitis
-Jaundice.
-Blumer’s shelf
-Virchow's node
-Sister Mary Joseph node
-Krukenberg tumor
-Irish node
Pathology
DIO Classification
Lauren Classification:
1. Intestinal Gastric ca.
It arises in areas of intestinal metaplasia to form
polypoid tumors or ulcers.
2.
Diffuse Gastric ca.
It infiltrates deeply in the stomach without
forming obvious mass lesions but spreads widely in
the gastric wall “Linitis Plastica”
& it has much more worse prognosis
3. Mixed Morphology.
Morphology
•
•
•
•
Polypoid
Ulcerative
Superficial spreading
Linitis plastica
Gastric cancer can be divided into:
 Early:
 Limited to mucosa & submucosa with or without
LN (T1, any N)
 >> curable with 5 years survival rate in 90%.
 Advanced:
 It involves the Muscularis.
 It has 4 types( Bormann’s classification). Type III &
IV are incurable.
Spread
Stagingof
ofGastric
gastric Cancer
cancer
T1 lamina
propria & submucosa
Direct Spread
Lymphatic spread
T2 muscularis & subserosa
Tumor penetrates the
What is important here is
T3
serosa
muscularis, serosa &
Virchow’s node
Adjacent
organs organs
T4
Adjacent
(Trosier’s sign)
(Pancreas,colon &liver)
N0
N1
N2
no lymph node
Blood-bornenode
Epigastric
metastasis
main arterial trunk
Usually with extensive
M0
Nowhere
distal
Disease
livermetastasis
1st
Involved
then metastasis
lung &
M1
distal
Bone
Transperitoneal
spread
This is common
Anywhere in peritoneal cavity
(Ascitis)
Krukenberg tumor (ovaries)
Sister Joseph nodule
(umbilicus)
Complications
 Peritoneal and pleural effusion
 Obstruction of gastric outlet or small bowel
 Bleeding
 Intrahepatic jaundice by hepatomegaly
Differential Diagnosis
1.Gastric ulcer
From history,
Cancer is not relieved by antacids
Not periodic
Not relieved by eating or vomiting.
2.Other gastric neoplasms
3.Gastritis
4.Gastric Polyp
5.Crohns disease.
INVESTIGATIONS
Full blood count –IDALFT,RFT
Amylase & lipase.
Serum tumor markers (CA 72-4,CEA,CA199) not specific
Stool examination for occult blood
CXR ,Bone scan.
Specific:
UGI endoscopy with biopsy
Double contrast study
CT, MRI & US
Laparoscopry
EGD esophagogastroduodenoscopy
Diagnostic accuracy is 98%
if up to 7 biopsies is taken.
Diagnostic study of Choice
Double Contrast barium upper GI x-ray
Diagnostic accuracy 90%
WHY?
1.Early superficial gastric mucosal lesion
can be missed.
2. can’t differentiate b/w benign ulcer &
Ulcerating adenocarcinoma.
X-ray showing Gastric ulcer
With symmetrical radiating
Mucosal folds.
By histology, no evidence of
Malignancies was observed.
X-ray showing Extensive
carcinoma involving
the cardia & Fundus
Pyloric stenosis
CT,MRI & US:
Help in assessment of wall thickness,
metastases (peritoneum ,liver & LN)
Laparoscopy:
Detection of peritoneal
metastases
UGI ENDOSCOPY
THE GOLD STANDARD
 It allows taking biopsies
 Safe (in experienced hands)
UGI ENDOSCOPY,contd.
 You may see an ulcer (25%),
polypoid mass (25%), superficial
spreading (10%),or infiltrative
(Linitis plastica)-difficult to be
detected Accuracy 50-95% it depends on
gross appearance, size, location &
no. of biopsies
IF YOU SEE ULCER ASK UR
SELF…BENIGN OR MALIGNANT?
BENIGN
MALIGNANT
Round to oval punched out
lesion with straight walls &
flat smooth base
Smooth margins with
normal surrounding
mucosa
Mostly on lesser curvature
Irregular outline with
necrotic or hemorrhagic
base
Irregular & raised margins
Majority<2cm
Any size
Normal adjoining rugal
folds that extend to the
margins of the base
Prominent & edematous
rugal folds that usually do
not extend to the margins
Anywhere
Management
• Surgery
• Chemotherapy
NO PROVEN BENEFIT
• Radiotherapy
Treatment
Initial treatment:
1.Improve nutrition if
needed by
parenteral or enteral
feeding.
2.Correct fluid
&electrolyte
& anemia if they are
present.
Preoperative Care
Preoperative Staging is
important because we
don’t want to subject
the patient to radical
surgery that can’t help
him.
PRE-OPERATIVE CARE
 Careful preoperative staging
 Screen for any nutritional deficiencies
& consider nutritional support
 Symptomatic control
 Blood transfusion in symptomatic
anemia
 Hydration
 Prophylactic antibiotics
 ABO & cross match
 Ask about current medications &
allergies
 Cessation of smoking
BASIC SURGICAL PRINCIPLES
3 TYPES:
TOTAL,SUBTOTAL,PALLIATIVE
 ANTRAL DISEASESUBTOTAL
GASTRECTOMY
 MIDBODY & PROXIMAL TOTAL
GASTRECTOMY
TOTAL (RADICAL) GASTRECTOMY
o Remove the stomach +distal part
of esophagus+ proximal part of
duodenum + greater & lesser
omentum + LN
o Oesophagojejunostomy with rouxen-y .
SUBTOTAL GASTRECTOMY
Similar to total one except that the
PROXIMAL PART of the stomach
is preserved
Followed by reconstruction &
creating anastomosis
( by gastrojejunostomy, Billroth II )
PALLIATIVE SURGERY
• For pts with advanced (inoperable)
disease & suffering significant
symptoms e.g. obstruction,
bleeding.
• Palliative gastrectomy not
necessarily to be radical, remove
resectable masses & reconstruct
(anastomosis/intubation/stenting/
recanalisation)
POSTOPERATIVE ORDERS
• Admit to PACU
• Detailed nutritional advise (small
frequent meals)
Post-Operative Complications
1.Leakage from
duodenal stump.
2.Secondary
hemorrhage.
3.Nutritional
deficiency in long
term.
2.Chemotherapy:
Responds well, but there is no effect on survival.
Marsden Regimen
Epirubicin, cisplatin &5-flurouracil (3 wks)
6 cycles
Response rate : 40% .
3. Radiotherapy:
Postperative-radiotherpy: may decrease the
recurrence.
Preventive measures
By diet
Convincing:
Early diagnosis
vegetable
& fruits. remains the Key
Probable:
Problem
Vit. C &E
Possible
Carotenoids, whole grain cereals and
green tea.
Smoking cessation
Cessation of alcohol intake
PROGNOSTIC FEATURES
2 important factors influencing survival in
resectable gastric cancer:
 depth of cancer invasion
 presence or absence of regional LN
involvement
• 5yrs survival rate:
10% in USA
50% in Japan
Bailey & Love’s short practice of
surgery
Clinical surgery ( A. Cuschieri).
E-medicine web site
The Washington Manual of
Surgery