GASTRIC

CANCER
ANATOMY

 Portions of the stomach

a. The cardia is the most proximal portion of the stomach, where it attaches
to the esophagus.
Immediately rostral to this area is the gastroesophageal {GE) junction. This
transition zone is found 2-3 cm below the diaphragmatic esophageal hiatus
and contains the lower esophageal sphincter mechanism.
b. The fundus is the most superior extension of the stomach, bounded by
the diaphragm superiorly and the spleen laterally. The angle created by the
fundus and the left lateral border of the esophagus is referred to as the
angle of His.
c. The body, also referred to as the corpus, is the largest portion of the
stomach. It consists of the lesser and greater curves. The incisura angularis
creates an abrupt angle along the lesser curvature and marks the beginning
of the antrum.
d. The antrum is the distal 25% of the stomach. It begins at the incisura
angularis and ends at the pylorus.
ARTERIAL SUPPLY

 The stomach has an extremely rich blood supply,

provided by the following vessels:
 a. The left gastric artery (branch of celiac axis)
supplies the lesser curvature (proximal).
 b. The right gastric artery (branch of common hepatic
artery} supplies the lesser curvature (distal).
 c. The left gastroepiploic artery (branch of the splenic
artery) supplies the greater curvature (proximal).
 d. The right gastroepiploic artery (branch of
gastroduodenal artery) supplies the greater curvature
(distal).
 e. The vasa brevia (short gastric arteries arising from
the splenic artery) supply the fundus and body.
VENOUS DRAINAGE

 Venous drainage of stomach in general parallels the

arterial supply but has some portal drainage.
 a. The right gastric and left gastric (coronary) veins
drain into the portal vein, while the right
gastroepiploic vein drains into the superior
mesenteric vein, and the left gastroepiploic vein
drains into the splenic vein.
 b. The left gastric vein (coronary vein) has multiple
anastomoses with the lower esophageal venous
plexus. These drain systematically into the azygous
vein.
LYMPHATIC
DRAINAGE
 Divided into four general zones.
 It is important to note that cancer
anywhere in the stomach can spread
equally to any zone.
 a. Superior gastric nodes drain the upper
lesser curve and cardia region.
 b. Pancreaticolienal nodes drain the
upper great curve and splenic nodes.
 c. Suprapyloric nodes drain the antral
segment of the stomach.
 d. Inferior gastric/subpyloric nodes drain
along the right gastroepiploic vessels.
ANATOMY
 The four layers of the stomach wall are the serosa, muscularis, submucosa, and mucosa.
a. The layers of muscle fibers found in the muscularis are the inner oblique, middle circular, and outer longitudinal
b. The mucosal morphology is composed of distinctly different types of glands unique to the cardia, fundus/body, and pylorus/antrum.
 (1) Cardiac glands occupy a narrow zone up to 4 cm long adjacent to the LES. These glands function mainly in producing mucus.
 (2) The fundus and body contain gastric glands with specialized cell types.
 (a) Mucous cells provide an alkaline coating for the epithelium. This coating facilitates food passage and provides some mucosal protection.
 (b) Chief cells are found deep in the fundic glands. They secrete pepsinogen, which is the precursor to pepsin. Pepsin is active in protein digestion.
Chief cells are stimulated by cholinergic impulses, gastrin, and secretin.
 (c) Oxyntic or parietal cells are found exclusively in the fundus and body of the stomach.
 They are stimulated by gastrin to produce hydrochloric acid as well as intrinsic factor.
 (3) The pyloroantral mucosa is found in the antrum of the stomach.
 (a) Parietal and chief cells are absent here.
 (b) G cells, which secrete gastrin, are found in this area. They are part of the amine precursor uptake and decarboxylase system of endocrine cells.
Gastrin stimulates hydrochloric acid and pepsinogen secretion and gastric motility.
ANATOMY
INNERVATION OF THE STOMACH

 Innervation of the stomach is via parasympathetic and sympathetic fibers.

 a. The vagus (parasympathetic) nerves stimulate parietal cell secretion, gastrin release, and gastric motility.
Acetylcholine is the primary neurotransmitter used by the efferent fibers.
 (1) The left vagus nerve lies anterior to and left of the esophagus. It supplies branches to the anterior portion of the
stomach and a hepatic branch to the liver, gallbladder, and biliary tree.
 (2) The right vagus nerve lies posterior to and right of the esophagus. It supplies branches to the posterior stomach
and a celiac branch to the pancreas, small bowel, and right colon. Its first branch is called the criminal nerve of
Grassi and is recognized as a cause of recurrent ulcer when left undivided.
 (3) The vagus nerves become the anterior and posterior nerves of Latarjet, which terminate at the pylorus as the
"crow's foot."
 b. Sympathetic innervation is via the greater splanchnic nerves derived from spinal segments T5 through T10.
These fibers terminate in the celiac ganglion, and postganglionic fibers follow the gastric arteries to the stomach.
The afferent fibers are the pathway for perception of visceral pain.
GASTRIC CANCER
 Gastric cancer is one of the most common causes
of cancer death in the world
 The outlook is generally poor, owing to the
advanced stage of the tumour at presentation
 Better results are obtained in Japan, which has a
high population incidence, screening programmes
and a high quality surgical treatment
 Approximately 90%-95% of gastric tumors are
malignant, and of the malignancies, 95% are
adenocarcinomas. Other histologic types include
gastrointestinal stromal tumor (GIST), lymphoma,
and carcinoid (rare).
 Incidence: more common in males; peak incidence between 5 th and 7th decade
 Third leading cause of cancer death worldwide
 Common in Japan
 Carcinoma of the distal stomach and body of the stomach is most common in low socioeconomic
groups, whereas the increase in proximal gastric cancer seems to affect principally higher
socioeconomic groups.
 Proximal gastric cancer does not seem to be associated with H. pylori infection, in contrast with
carcinoma of the body and distal stomach.

EPIDEMIOLOGY
 ETIOLOGY
Risk factors:
 Helicobacter pylori infection, (intestinal type Ca)
 Dietary Factors – High salt
 Precancerous conditions: foods, smoked meats that
-Adenomatous gastric polyps (sessile type)
-Previous gastric operations, contain high levels of nitrate.
-Pernicious anemia,  Tobacco use
-Atrophic gastritis,
-Menetrier’s disease  Alcohol use
 Hereditary and Genetic Factors –
 Hereditary diffuse gastric cancer (HDGC) (diffuse type)
 Family history
- Gene mutation for cell adhesion molecule E-cadherin.
 Male gender
 HNPCC or Lynch syndrome  Obesity
 Familial adenomatous polyposis mutations.
 Mutation in tumor suppressor genes p53 and p16
Adenocarcinoma (95% of cases)
• Typically localized, exophytic lesion +/-
ulceration
• Arise from glandular cells in the stomach; usually
located on the lesser curvature of the stomach PATHOLOGY
Signet ring cell carcinoma
• Diffuse growth
• Multiple signet ring cells = round cells filled
with mucin, with a flat nucleus in the cell
periphery
PATHOLOGIC CLASSIFICATION (MACROSCOPIC)

Classification of advanced gastric cancer according to

Borrmann:
Type I: polypoid fungating,
Type II: ulcerative with elevated distinct borders, Protruded type
Type 1
Type III: ulcerative with indistinct borders,
Type IV: diffuse, indistinct borders (Linitis plastica) Type 2

Type 3 Depressed type

Type I and II: localized types,
Types III and IV: infiltrative Types. Type 4
LAUREN
CLASSIFICATION
PATHOGENESIS

Intestinal type Diffuse type

“Preneoplastic-Cascade” • No defined series of preneoplastic stages
1. Chronic non-atrophic gastritis • No clearly defined preneoplastic lesions
2. Atrophic gastritis • Defective intercellular adhesions:
3. Intestinal Metaplasia E-cadherin
4. Dysplasia (intraepithelial neoplasia) • Individual tumor cells invade the surrounding tissues
5. Invasive carcinoma
JAPANESE
CLASSIFICATION
 Type I : Protruded type
 Type IIa : Superficial
elevated type
 Type IIb : Flat type
 Type IIc : Superficial
depressed type
 Type III : Excavated type
 “ALARM FEATURES” SUGGESTIVE OF GASTRIC CANCER

 New onset dyspepsia in patients >55 years of age

 Family history of UGI cancer
 Unintentional weight loss
 Upper or lower GI bleeding
 Progressive dysphagia
 Iron deficiency anaemia
 Persistent vomiting
 Palpable mass
 Palpable lymph nodes
 SIGNS AND SYMPTOMS

 Epigastric pain (constant, nonradiating, exacerbated by food)

 Early satiety, nausea, vomiting
 Weight loss
 With more advanced lesions: obstruction, dysphagia (depending on the location of the
tumor), GI bleeding resulting in anemia (40%) and hematemesis (15%)
 Paraneoplastic syndromes:
1.Acanthosis Nigricans
2.Leser-Trelat sign (multiple seborrheic keratosis)
PARANEOPLASTIC SYNDROMES

Acanthosis nigricans Leser-Trelat sign

METASTASES

 Krukenberg’s tumor—metastasis to ovaries.

 Blumer’s shelf—metastasis to pelvic cul-de-sac, felt on digital rectal exam.
 Virchow’s node—metastasis to lymph node palpable in left supraclavicular fossa.
 Sister Mary Joseph’s nodule—periumbilical metastatic nodules.
 Intraabdominal metastases (hepatomegaly, jaundice, or ascites)
 DIAGNOSIS
 Esophagogastroduodenoscopy: Best method,
allows for biopsy, definitive > 95% sensitivity and
specificity.
 Upper GI series: With double contrast; 80–96%
sensitivity, 90% specificity (operator dependent);
excellent method in skilled hands.
 Abdominal CT: Good for detecting distant
metastases; also used for preop staging, but
suboptimal.
 Endoscopic ultrasound: Good for detecting depth
of invasion.
 Diagnostic laparascopy
 Markers may be elevated in the setting of gastric
cancer, including carcinoembryonic antigen (CEA),
CA-125, CA 19-9, and β-HCG. These biomarkers,
however, lack sufficient sensitivity and specificity
to establish a diagnosis.
TNM STAGING
  Direct spread:
Tumor penetrates the muscularis, serosa &
adjacent organs (Pancreas ,colon &liver)
 Lymphatic spread:
What is important here is Virchow’s node
(Trosier’s sign)

Blood-borne metastasis:

SPREAD Usually with extensive disease where the liver is

involved 1st then lung & Bone

Transperitoneal spread:
Anywhere in peritoneal cavity (Ascites)
Krukenberg tumor (ovaries) Sister Joseph nodule
(umbilicus)
TREATMENT

Exact therapy, which may be either curative or palliative, depends on staging and the type
of tumor.
• Endoscopic mucosal resection
• Surgery
• Perioperative chemotherapy, sometimes radiotherapy
• Newer biological agents such as trastuzumab (Herceptin®) offer potential advantages to
survival in the minority of patients (<20 per cent) with HER2-positive gastric cancer
SURGERY

 Radical gastrectomy and lymphadenectomy (operative standard)

 Resection of the lesser and greater omentum and radical lymphadenectomy
 Roux-en-Y gastric bypass
 The surgeon separates the proximal jejunum from the duodenum and creates an end-to-
side anastomosis of the jejunum with the remaining part of the stomach (gastrojejunostomy), or in the
case of a total gastrectomy, end-to-end anastomosis with the esophagus (esophagojejunostomy).
 Duodenal stump is connected distally with the jejunum using an end-to-side anastomosis.
 Alternative: subtotal gastrectomy (reconstruction methods: Bilroth I/II or Roux-en-Y gastrojejunostomy)
 Palliative surgery: palliative gastrectomy does not need to be radical; it is sufficient to remove the tumour and
reconstruct the gastrointestinal tract.
Radical gastrectomy Subtotal gastrectomy
  Related to resorption
• Malabsorption
• Consequences and management
POSTGASTRECTOM • Iron deficiency → supplement iron
Y SYNDROMES • Pernicious anemia due to lack of intrinsic factor,
usually produced by gastric parietal cells →
supplement vitamin B12
  Related to anastomosis
• Small intestinal bacterial overgrowth (SIBO)
• Definition: bacterial overgrowth within the small intestine
• Causes
• Anatomic abnormalities: (e.g., surgery causing blind
intestinal loops – blind loop syndrome, strictures)
• Motility disorders
POSTGASTRECTOM • Clinical features: diarrhea, steatorrhea, weight
Y SYNDROMES loss, malabsorption (e.g., deficiency of vitamin B12, A, E,
D, zinc, and iron)
• Diagnostics
• Jejunal aspirate cultures collected during endoscopy
• Positive lactulose breath test
• Treatment: antibiotics and parenteral
supplementation of vitamins and proteins, possibly surgical
treatment
  Related to motility
• Dumping syndrome: rapid gastric emptying due to either defective gastric reservoir function or pyloric emptying
mechanism, or anomalous post-surgery gastric motor function.
Early
 Timing: occurs minutes after a meal
 Etiology: rapid gastric emptying of hyperosmolar chyme into small bowel causes rapid fluid shifts
 Symptoms: postprandial tachycardia, diaphoresis, abdominal pain, and diarrhea
 Incidence: occurs in 75% of patients after gastric surgery, more common after BII vs. BI
Late

POSTGASTRECTOM  Timing: occurs hours after a meal


Y SYNDROMES 
Etiology: hyperosmolar chyme causes hyperglycaemia → insulin hypersecretion → hypoglycaemia.
Symptoms: palpitations, weakness, sweating, and dizziness
Diagnosis
 UGI contrast study
Treatment
 Majority of cases resolved with conservative dietary and medical management
 Dietary: small meals, no liquids with food, and limit sugars
 Somatostatin: inhibits vasoactive peptides and slows transit time
 Surgery: convert BI or BII to Roux-en-Y; used for serious dumping syndrome; increase gastric reservoir with a
jejunal pouch or increase emptying time (reversed jejunal loop)
  Prognosis depends largely on the depth of invasion of the
gastric wall, involvement of regional nodes, and presence
of distant metastases but still remains poor.
 Overall 5-year survival after the diagnosis of gastric cancer
is 10%-20%.
 Tumors not penetrating the serosa and not involving
regional nodes are associated with a 5-year survival rate of
PROGNOSIS approximately 70%. This number decreases dramatically if
the tumor is through the serosa or into regional nodes.
 Recurrence rates after gastric resection are high, ranging
from 40%-80%.
 Potentially curative surgical resection does offer a better 5-
year prognosis; however, only 40% of patients have
potentially curable disease at the time of diagnosis.
 GASTRIC LYMPHOMA
The stomach is the most common site of primary intestinal lymphoma; however, gastric lymphoma is relatively uncommon, accounting
for only 15% of all gastric malignancies and only 2% of lymphomas.
I. Symptoms are usually vague, namely abdominal pain, early satiety, and fatigue. Rarely ever do patients present with constitutional
symptoms (i.e. "B" classification of lymphoma). Patients at risk for developing lymphomas are those who are immunocompromised or
are harbouring an H. pylori infection.
2. Diagnosis consists of endoscopy with biopsy and endoscopic ultrasound for staging. As with all lymphomas, assessment of distant
disease should include bone marrow biopsy; CT of chest, abdomen, and pelvis; as well as an upper airway exam. Testing for H. pylori
should also be performed.
3. Treatment consists of a multimodality regimen, with the role of gastric resection remaining highly controversial.
a. Medical treatment combining chemotherapy and radiation is now the most accepted first line therapy for treating gastric lymphoma.
The most common chemotherapy combination is cyclophosphamide, hydroxydaunomycin, Oncovin, and prednisone (CHOP). Some
variants of lymphoma may also be treated effectively by the eradication of H. pylori infection alone.
b. Surgical treatment is now used mostly for the complications of bleeding and perforation that arise from locally advanced disease. The
treatment involves the removal of all gross disease via partial gastrectomy.
4. Prognosis is good, with a 5-year survival greater than 95% when disease is localized to the stomach and 75% when local lymph
nodes are involved.
GASTRIC SARCOMAS

Gastric sarcomas arise from the mesenchymal cells of the gastric wall and constitute 3% of all gastric cancers.
Gastrointestinal stromal tumors (GIST) are the most common and are found predominately in the stomach.
1. Gastrointestinal stromal tumors (GIST) arise from mesenchymal cells of the GI tract, usually the pacemaker cell
of Cajal.
2. Histologic diagnosis is confirmed by immunohistochemical staining for CD 117, a cell surface antigen.
3. Presentation varies from incidental asymptomatic endoscopy or CT findings to symptomatic large tumors causing
obstruction, pain, bleeding, or metastases.
4. Treatment is complete surgical removal. Clinical behavior and malignant potential are based on several factors,
including mitotic count >5 per 50 high-power fields; size >5 cm; and cellular atypia, necrosis, or local invasion.
Tumor recurrence or unresectable disease can be treated by imatinib mesylate (Gieevec), which inhibits the c-
KIT gene-associated tyrosine kinase receptor responsible for tumor growth. Overall 5-year survival is 50%.
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