Gastric Cancer

OLEH: dr.HANS MARPAUNG,

SpB,FICS

The management of gastric cancer requires

a thorough understanding of gastric
anatomy.
The stomach begins at the
gastroesophageal junction and ends at the
duodenum.
The stomach has 3 parts.
-cardia,
-the body.
-the pylorus, connects to the
duodenum.
The cardia contains predominantly mucinsecreting cells.
The fundus (ie, body) contains mucoid cells,
chief cells, and parietal cells.

The site of the lesion

-40% of cancers develop in the
lower part
-40% in the middle part
-15% in the upper part
-10% involve more than one part of
the
organ.

The stomach wall is made up of 5 layers.

-the mucosa
-the submucosa
- muscular layer
-subserosal layer
- serosal layers.
The peritoneum of the greater sac covers the
anterior surface of the stomach.
A portion of the lesser sac drapes posteriorly over the
stomach.
The gastroesophageal junction has limited or no
serosal covering. The right portion of the anterior
gastric surface is adjacent to the left lobe of the liver
and the anterior abdominal wall.
The left portion of the stomach is adjacent to the
spleen, the left adrenal gland, the superior portion of
the left kidney, the ventral portion of the pancreas,

Pathophysiology:

Celiac artery a branch

left gastric artery upper right portion of the
stomach.
common hepatic artery a branch
1.right gastric artery lower portion of the stomach
2.right gastroepiploic branchlower portion of the
greater curvature.

lymphatic drainage for nodal involvement by

cancer.
The lymphatic drainage of the stomach is complex.
Primary lymphatic drainage is along the celiac axis.
Minor drainage occurs along the
-splenic hilum
-suprapancreatic nodal groups

Spread patterns
Cancer of the stomach can spread :
-directly,
-via lymphatics,
- hematogenously.
Direct extension into :
- the omenta
- pancreas
- diaphragm
- transverse colon or mesocolon
-duodenum
If the lesion extends beyond the gastric wall to
a free peritoneal (ie, serosal) surface, then
peritoneal involvement is frequent.

. Lymphatic drainage of the stomach. (From Moody F, McGreevy J, Miller T:

. Lymphatic drainage of the stomach. (From Moody F, McGreevy

J, Miller T: Stomach. In Schwartz SI, Shires GT [eds]: Principles
of Surgery, 5th ed. New York, McGraw-Hill, 1989.)

Lymph node station numbers as defined by the Japanese Gastric Cancer Association.
(From Japanese Gastric Cancer Association: Japanese Classification of Gastric
Carcinoma2nd English Edition. Gastric Cancer 1:10-24, 1998.)

History:
Early disease has no associated symptoms
Most symptoms of gastric cancer reflect advanced
disease.
Patients may complain of
-indigestion
-nausea or vomiting
-dysphagia
-postprandial fullness
-loss of appetite, and weight loss.
Late complications
-pathologic peritoneal and pleural effusions
-obstruction
-bleeding in the stomach
-intrahepatic jaundice caused by
hepatomegaly; -extrahepatic jaundice
-starvation or cachexia of tumor origin.

Signs
1.palpable enlarged stomach with succussion splash
2.Hepatomegaly
3.Sister Mary Joseph nodule periumbilical
metastasis
4. Virchow nodes left supraclavicular nodes
5.Irish node anterior axillary node
6.Blumer shelf (ie, shelflike tumor of the anterior
rectal wall).
7.Some patients experience weight loss and others
may present with melena or pallor from anemia.

Causes:
Several factors are implicated in the
development of gastric cancer, including :
-diet
- Helicobacter pylori infection
- previous gastric surgery
-pernicious anemia,
-adenomatous polyps,
-chronic atrophic gastritis,
-genetic factors
- previous radiation therapy.
Gastric cancer most likely represents the
result of multiple events occurring in an
appropriate environment.

Diet
increased incidence of gastric cancer.
pickled vegetables
salted fish
excessive dietary salt
smoked meats
protective effect.
-fruits and vegetables rich in
vitamin C
Helicobacter pylori infection

Previous gastric surgery

Previous surgery is implicated as a risk factor.
The rationale is that surgery alters the normal pH
of the stomach.
Retrospective studies demonstrate that a small
percentage of patients who undergo gastric polyp
removal have evidence of invasive carcinoma
within the polyp. This discovery has led some
researchers to conclude that polyps might
represent premalignant conditions.
Genetic factors
Genetic factors involved in gastric cancer remain
poorly understood.
Certainly some familial aggregation exists.

Risk factors for gastric cancer include

Helicobacter pylori gastric infection.
Advanced age.
Male gender.
Diet low in fruits and vegetables.
Diet high in salted, smoked, or preserved foods.
Chronic atrophic gastritis.
Intestinal metaplasia.
Pernicious anemia.
Gastric adenomatous polyps
Family history of gastric cancer.
Cigarette smoking.
Menetriers disease (giant hypertrophic gastritis).
Blood group A
Familial adenomatous polyposis.

Lab Studies:
The goal of obtaining laboratory studies is to assist
in determining optimal therapy.
A complete blood cell count can identify anemia,
which may be caused by bleeding, liver
dysfunction, or poor nutrition. Approximately 30%
of patients have anemia.
Electrolyte panels and liver function tests also are
essential to better characterize the patient's clinical
state.

Imaging Studies:

Esophagogastroduodenoscopy
This relatively safe and simple procedure
provides a permanent color photographic record

 Double-contrast upper GI series

An upper gastrointestinal barium swallow detects
large primary tumors but only occasionally
detects their spread to the esophagus and
duodenum (particularly if the tumor is small and
submucosal).
The smaller the primary lesion, the more
important is the use of double-contrast and
cineradiography.
Chest radiograph: This is done to evaluate for
metastatic
lesions.
CT scan or MRI of the chest, abdomen, and pelvis
These imaging studies assess the local disease
process as well as evaluate potential areas of
spread (ie, enlarged lymph nodes, possible liver
metastases).
Some patients' tumors are judged surgically

Endoscopic ultrasound
This study allows f or a more precise
preoperative assessment of the tumor
stage.
Endoscopic sonography is becoming
increasingly useful as a staging tool when
the CT scan fails to find evidence of T3, T4,
or metastatic disease.
Institutions that favor neoadjuvant
chemoradiotherapy for patients with
locally advanced disease rely on
endoscopic ultrasound data to improve
patient stratification.

Histologic Findings:
Adenocarcinoma of the stomach constitutes
between 90% and 95% of all gastric
malignancies.
The second most common gastric malignancies
are lymphomas. Leiomyosarcomas (2%),
carcinoids (1%), adenoacanthomas (1%), and
squamous cell carcinomas (1%) are the
remaining tumor histologic types.
Adenocarcinoma of the stomach is classified
according to microscopic criteria. Classification
is based on the most unfavorable microscopic
element present, which are, in order of
increasing danger, tubular, papillary, mucinous,
or signet-ring cells, and undifferentiated lesions.
Pathology specimens also are classified by gross

The Borrmann system has 5

categories:
1.type I tumors are polypoid or
fungating;
2. type II are ulcerating lesions
surrounded by elevated borders;
3.type III have ulceration with
invasion of the gastric wall;
4.type IV are diffusely infiltrating (ie,
linitis plastica);
5.type V cannot be classified.

Gross classification of gastric cancer. Gastric cancer can be polypoid, ulcerating, or

infiltrating. Linitis plastica is the infiltrating type with the poorest survival outcome.
(Adapted from Douglass HO, Nava HR. Gastric adenocarcinomamanagement of
the primary disease. Semin Surg Oncol 1985;12:3245.)

Staging: The 1997 American Joint Committee on Cancer (AJCC)

Cancer Staging Manual presents the following TNM classification
system for staging gastric carcinoma:
Primary tumor
TX = primary tumor (T) cannot be assessed
T0 = no evidence of primary tumor
Tis = carcinoma in situ, intraepithelial tumor without invasion of
lamina propria
T1 = tumor invades lamina propria or submucosa
T2 = tumor invades muscularis propria or subserosa
T3 = tumor penetrates serosa (ie, visceral peritoneum) without
invasion of adjacent structures
T4 = tumor invades adjacent structures
Regional lymph nodes
NX = regional lymph nodes (N) cannot be assessed
N0 = no regional lymph node metastases
N1 = metastasis in 1-6 regional lymph nodes
N2 = metastasis in 7-15 regional lymph nodes
N3 = metastasis in more than 15 regional lymph nodes
Distant metastasis
MX = distant metastasis (M) cannot be assessed
M0 = no distant metastasis

The 2006 American Joint Committee on Cancer (AJCC ) stage groupings

Stage 0
Tis, N0, M0
Stage IA
T1, N0, M0
Stage IB

Stage II
T1, N2, M0
T2a, N1, M0
T2b, N1, M0
T3, N0, M0

Stage IIIA
T2a, N2, M0
T2b, N2, M0
T3, N1, M0
T4, N0, M0

Stage IV
T4, N1, M0
T4, N2, M0
T4, N3, M0
T1, N3, M0
T2, N3, M0
T3, N3, M0
Any T, any N,
M1

T1, N1, M0
T2a, N0, M0
T2b, N0, M0

Stage IIIB
T3, N2, M0

NX: Regional lymph node(s) cannot

be assessed
N0: No regional lymph node
metastasis*
N1: Metastasis in 1 to 6 regional
lymph nodes
N2: Metastasis in 7 to 15 regional
lymph nodes
N3: Metastasis in more than 15

TX: Primary tumor cannot be assessed

T0: No evidence of primary tumor
Tis: Carcinoma in situ: intraepithelial tumor without
invasion of the lamina propria
T1: Tumor invades lamina propria or submucosa
T2: Tumor invades the muscularis propria or the
subserosa
T2a: Tumor invades muscularis propria
T2b: Tumor invades subserosa
T3: Tumor penetrates the serosa (visceral peritoneum)
without invading adjacent structures
T4: Tumor invades adjacent structures

Staging and 5-Year Survival Rates

Stage

TNM Stage

5-Year Survival

T1N0M0, T1N1M0,
or T2N0M0

88%

T1N2M0, T2N1M0,
or T3N0M0

65%

3a

T2N2M0, T3N1M0,
or T4N0M0

35%

3b

T3N2M0

35%

T4N1-3M0,
TxN3M0, or
TxNxM1*

5%

Prognostic features
Two important factors influencing
survival in resectable gastric cancer
are :
-depth of cancer invasion through
the
gastric wall
-presence or absence of regional
lymph
node involvement.

Management
Early gastric cancer (10%)
Cancer is limited to mucosa and submucosa
Aggressive treatment with resection. Curative treatment
(resectable primary and local nodes) involves surgical
excision with clear margins and locoregional lymph node
clearance (D2 gastrectomy)
With adequate resection, prognosis is good (80% 5-year
survival)
Advanced gastric cancer (90%)
Cancer involves muscularis propria of the stomach wall
Majority of tumours are unresectable at presentation
Palliation (metastatic disease or gross distal nodal disease
at presentation):
(a) Gastrectomy: local symptoms, e.g. bleeding
(b) Gastroenterostomy: malignant pyloric obstruction
(c) Intubation: obstructing lesions at the cardia

- Other treatment: combination chemotherapy with etoposide,

Adriamycin and cisplatin may induce regression.
- Most tumours are poorly responsive to chemotherapy
- Prognosis: overall 5-year survival (palliation and resection)
is only about 5%

Palliative Treatment
Occasionally, palliative gastrectomy is required to treat
bleeding or obstruction, even though tumor may be left
behind. At other times, gastroenterostomy is performed
to bypass an obstructing distal gastric cancer.
Obstructing tumors at the cardia may be palliated by
endolaser therapy.

Palliative bypass
This type of operation is
design principally for
advanced distal gastric
tumours that are
unresectable fore cure and
fixed to vital structures
such as the CBD or mayor
vessel or pancreas. Bypass
is achieved by
anastomosing the small
bowel (jejunum) to the
stomach proximal to the
obstruction lesion

Distal GastricTumour

Adjuvant Therapy
Carcinoma of the stomach is poorly
responsive to chemotherapy or
radiotherapy