Gastric cancer arises from the cells lining the stomach. It is most commonly adenocarcinoma, which can be intestinal or diffuse type. Risk factors include H. pylori infection, smoking, and family history. Symptoms often do not appear until late stages, when they may include abdominal pain, weight loss, vomiting, or bleeding. Diagnosis involves endoscopy with biopsy. Treatment depends on stage but may include surgery, chemotherapy, and radiation. Prognosis is best if caught early before spread, but late-stage gastric cancer generally has a poor prognosis.
2. 01 INTRODUCTION
02 ANATOMY
03 CLASSIFICATION
04 ADENOCARCINOMA
05 OTHER TUMORS
06 RISK FACTORS
07 SYMPTOMS
08 OTHER SYMPTOMS
09 DIAGNOSIS
CONTENTS:
10 WORKUP OF DIAGNOSED GASTRIC CANCER
11 PROGNOSIS
12 TREATMENT
13 SURGERY
14 POST GASTRECTOMY COMPLICATIONS
15 DIFFERENTIAL DIAGNOSIS
16 PROGNOSIS
17 RESOURCES
3. 01 INTRODUCTION
• Stomach cancer, also known as gastric
cancer, is a cancer that arises from the
cells lining the stomach.
• Generally gastric cancer is considered
a poor prognosis cancer, because it
doesn’t cause specific symptoms until
later stages.
• Incidence: Male > Female
6. Gastric cancer can appear in any part of the
stomach and is classified into:
Adenocarcinoma
- orginates from columnar glandular
epithelium
Lymphoma
- orginates from lymphocytes
Carcinoid Tumor
- orginates from G-Cells in the stomach
Leiomyosarcoma
- orginates from muscle cells
03 CLASSIFICATION
7. Description
• Most common type of
gastric cancer
• Originates from columnar
glandular epithelium
Intestinal Type
• Well differentiated
• Most common cause:
Helicobacter pylori
Diffuse Type
• Undifferentiated
• Most common cause:
Mutations
04 ADENOCARCINOMA
Sub Types
8. INTESTINAL TYPE OF ADENOCARCINOMA
• Most common -
accounts for ∼
95% of cases
• Most commonly
located on the
lesser curvature
• Arises from
glandular cells in
the stomach
Pathology
• Typically localized
• Well differentiated
• Polypoid, glandular
formation
• Similar to an ulcerative
lesion with clear raised
margins
9. ● H pylori – releases virulence factors like cagA,
that goes inside epithelial cells and cause
extensive damage.
● The intestinal type of non-cardia gastric cancer is
generally thought to arise from Helicobacter
pylori infection, which initiates the immune system
that causes an inflammatory response, which
progresses from chronic non-atrophic gastritis to
atrophic gastritis, then intestinal metaplasia, and
finally dysplasia. This progression is known as
Correa’s cascade.
PATHOGENESIS
10. ● The stomach cells resemble the interstinal
epithelium during metaplasia, which in turn
accumulates mutations in the genes that are in
charge of the cell cycle and cell division.
● Tumor suppressor genes, which normally code
for proteins that stop the cell cycle or promote
apoptosis, are the cell cycle’s very own brake
pedal, while proto-oncogenes, which normally
code for proteins that promote the cell cycle, are
the cell cycle’s accelerator pedal.
● Mutations can occur in both, causing metaplastic
cells to divide uncontrollably with the mutations at
each division. These mutations also make the cell
malignant.
PATHOGENESIS
11. DIFFUSE TYPE OF ADENOCARCINOMA
• No clear border
• Spreads earlier in
the course of
disease
• Infiltrative growth
• Diffuse spread in
the gastric wall
Pathology
• Linitis plastica: gastric wall
thickening and leather bottle
appearance
• Composed of signet ring cells:
round cells filled with mucin, with a
flat nucleus in the cell periphery
• Associated with E-cadherin
mutation
12. ● Diffuse type of adenocarcinoma can appear in
any part of the stomach, and it is mostly related to
genetic mutations in the CDH1 gene, a tumor
suppressor gene that codes for a membrane
adhesion molecule called E-cadherin.
● Normally, E-cadherin helps epithelial cells stick to
one another and it also transmits signals that
control the progression of the cell cycle. When E-
Cadherin isn’t working properly, cells detach and
starts dividing uncontrollably. This type of
adenocarcinoma has an increased ability to
spread and invade adjacent structures, so it is
way more aggressive than the intestinal type.
PATHOGENESIS
13. ● Diffuse gastric cancer can appear in any part of
the stomach, and can cause gastric linitis or linitis
plastica, where the stomach wall grow thick and
hard, and look like a leather bottle.
● This is the result of diffuse adenocarcinoma
invading the connective tissue of the submucosa,
causing it to become thicker and more rigid.
● Histologically, there are signet ring cells scattered
throughout the connective tissue, as the
cytoplasm in these cells has giant vacuoles that
push the nucleus to the edge of the cell.
PATHOGENESIS
14.
15. 05 OTHER TUMORS (LESS COMMON)
LYMPHOMAS
• Arise mostly from lymphocytes found
in MALT (Mucosa-associated
lymphoid tissue)
• Chronic H-pylori infection causes
excessive B Cell proliferation, which
makes them more prone to mutations
and develop lymphoma.
• Appear as diffuse lymphocytes
surrounding normal lymphoid
nodules and epithelial cells.
16. 05 OTHER TUMORS (LESS COMMON)
CARCINOID TUMORS
• Arises from the neuroendocrine
cells, i.e, the G-cells of the stomach.
• It is a well differentiated tumor
arrising from the mucosa as a polyp.
• Can also arise in the intestine and
the pancreas, as they also contain
G-Cells.
17. 05 OTHER TUMORS (LESS COMMON)
• Arise from smooth muscle cells of
the gastic wall, and are extremely
rare.
• Under microscope, cancer cells can
look like spindle, epithelial or
undifferentiated cell.
LEIOMYOSARCOMA
18. EXOGENOUS ENDOGENOUS
• Diet rich in nitrates and/or
salts (e.g., dried foods, foods
preserved by curing or
smoking); and low in fresh
vegetables containing
antioxidants
• H. pylori infection
• Nicotine and alcohol use
• Epstein-Barr virus
• Low socioeconomic status
• Obesity
•
Gastric conditions:
• Chronic atrophic gastritis and associated pernicious
anemia
• Achlorhydria (e.g., due to Ménétrier disease)
• Gastric ulcers
• Partial gastrectomy
• Adenomatous gastric polyps
• Gastroesophageal reflux disease
Hereditary factors:
• Male gender
• Positive family history
• Blood type A
• Hereditary nonpolyposis colorectal cancer
06 RISK FACTORS
19. EARLY STAGES
• Often asymptomatic
• Malaise
• Loss of appetite
• Dyspepsia
General signs:
• Epigastric pain
• Nausea
• Vomiting
• Weight loss
07 SYMPTOMS
LATE STAGES
LATE STAGES
Signs of gastric outlet obstruction
• Dysphagia
• Abdominal pain
• Early satiety
• Vomiting
Signs of upper gastrointestinal bleeding
• Hematemesis
• Melena
20. Signs of metastatic disease:
- Hepatomegaly
- Ascites
- Palpable mass on digital rectal
examination (Blumer shelf)
- Ovarian mass (Krukenberg
tumor)
Paraneoplastic syndromes:
- Polyarthritis nodosa
08 OTHER SYMPTOMS
- Left supraclavicular
adenopathy- Virchow’s node
(Troisier’s sign) - Palpable umbilical nodule
(Sister Mary Joseph sign)
- Leser-Trélat sign
- Malignant acanthosis nigricans
21. Confirmatory tests:
● Upper endoscopy with biopsy (best initial and confirmatory
test)
● Upper GI series (barium studies): especially for linitis plastica
Laboratory tests:
● Complete blood count: anemia
● Fecal occult blood test: positive
● Renal and liver function tests
● Serologic markers-
-Tumor markers: CA 72-4, CA 19-9, CEA
-TNF-α
● Immunohistochemistry: HER2 testing
09 DIAGNOSTICS
22. Imaging
● Endosonography
- Depth of tumor invasion
- Lymph node involvement
● Abdominal ultrasound
● CT scan (abdomen, pelvis, and thorax)
- Lymph node involvement
- Detection of distant metastases
● PET-CT/diagnostic laparoscopy: for occult
metastases that could have been missed
during endoscopy or on CT scan
10 WORKUP OF DIAGNOSED GASTRIC
CANCER
25. 12 TREATMENT
Early-stage disease:
• Endoscopic tumor resection
• Subtotal or total gastrectomy (if any
lymph nodes are involved)
• H. pylori infection treatment
Late-stage disease:
• Perioperative chemotherapy or
radiotherapy
• Used as both neoadjuvant and
adjuvant therapy
• Trastuzumab is indicated for HER2-
positive gastric adenocarcinomas
26. 13 SURGERY
Total gastrectomy and lymphadenectomy
(operative standard)
• Complete resection of the stomach with
blind closure of the proximal duodenum
• Resection of the lesser and greater
omentum
• Radical lymphadenectomy
Subtotal gastrectomy (alternative approach)
• Resection of the body and pylorus of the
stomach with blind closure of the duodenal
stump
• Radical lymphadenectomy
27. 13 SURGERY
Roux-en-Y gastric bypass: a surgical technique used in the
reconstruction of the gastric passage and to prevent GI
obstruction after gastrectomy/bariatric surgery
• The jejunum is divided transversely just distal to the
duodenum and incised longitudinally further distally.
• Esophagojejunostomy creation: end-to-end
anastomosis between the distal esophagus (or
remaining part of the stomach; gastrojejunostomy) and
the distal limb of the transected jejunum
• Jejunojejunostomy creation: end-to-side anastomosis
between the proximal limb of the transected jejunum
and the transversely incised distal jejunum
28. 14 POST GASTRECTOMY COMPLICATIONS
• Malabsorption
• Small intestinal bacterial overgrowth (SIBO)
• Efferent Loop Syndrome
• Afferent Loop Syndrome
• Dumping syndromes: Early and late dumping
• Remnant gastric cancer
30. ● Because there are no early signs, gastric cancer is
often diagnosed very late. Around 50% of cancers
have already reached an advanced stage that does
not allow for curative treatment due to tissue invasion
and metastases.
● If diagnosed at a very early stage, the 5-year survival
rate is 95%.
● Late-stage disease with distant metastases and/or
peritoneal carcinomatosis has a poor prognosis (5-
year survival rate of ∼ 5%).
16 PROGNOSIS