Gastric Carcinoma

Meet the patient

A 62-year-old man spent four months telling his GP that food "sits heavy" after meals; the GP called it dyspepsia and pushed the PPI dose up. He has now lost 9 kg, looks pale, and examination finds a hard, fixed epigastric mass and a 2 cm firm node in the left supraclavicular fossa. The routine OGD booked for next month is, from this morning, a 2-week-wait.[1]

Two questions frame the whole topic, and every section below answers one of them: is the cancer still curable? — a question of stage, settled by depth, nodes, and the peritoneum — and has it already spread? — a question for CT, then for staging laparoscopy. Miss either question and you miss the patient.[1]

Overview & Definition

Gastric carcinoma is an adenocarcinoma of the gastric glandular epithelium, and about 95 per cent of all stomach malignancies are adenocarcinomas. The minority — MALT lymphoma, GIST, neuroendocrine tumours — are the differentials, not the disease.[1]

Most tumours are the endpoint of a slow, inflammatory pathway first drawn by the Colombian pathologist Pelayo Correa in 1975: chronic mucosal injury, usually from Helicobacter pylori, marches over 20 to 40 years through chronic gastritis, atrophic gastritis, intestinal metaplasia, dysplasia, and finally invasive adenocarcinoma.[2]

The clinical problem is lateness, full stop. The stomach is capacious and distensible, so an early tumour is silent or mimics peptic ulcer disease; patients arrive only once the tumour has invaded muscle, obstructed the lumen, or seeded the peritoneum. Global five-year survival sits at 20 to 30 per cent, yet a mucosa-confined tumour is curable in over 90 per cent of cases.[1]

That survival gap — Japan and Korea screen and catch mucosal disease; the West and South Asia present late — is the single most examined fact in gastric surgical oncology, and it is why the rest of this page exists.[1]

Four axes, one tumour — hold them all at once

A candidate who can place a gastric tumour on four axes can answer almost any classification question. Hold histology (Lauren), site, depth, and TNM simultaneously — each axis drives a different decision: prognosis, operation, adjuvant therapy.[1]

By histology — the Lauren classification (1965) is the exam favourite:[1]

• Intestinal type (Lauren 1) — gland-forming, well to moderately differentiated, an expanding, pushing margin; driven by H. pylori, salted/smoked diet, and chronic atrophic gastritis along the Correa cascade; predominates in older males in high-incidence regions; the better prognosis.
• Diffuse type (Lauren 2) — discohesive signet-ring cells (mucin shoves the nucleus aside) growing by infiltration; not clearly linked to H. pylori or diet; predominates in younger patients and women; the hereditary form driven by E-cadherin loss (CDH1). Diffuse infiltration of the whole wall is linitis plastica. Prognosis is poor.
• Mixed type — both glandular and signet-ring components.[1]

Etymology worth a viva mark: linitis plastica is Greek — linos (linen, leather) and plastikos (moulded) — the "leather bottle" stomach, rigid and non-distensible because signet-ring cells have infiltrated every layer. When the endoscope looks normal but the stomach will not insufflate, think leather bottle.[1]

The WHO scheme (tubular, papillary, mucinous, poorly cohesive) is what the pathologist reports; Lauren is what the examiner asks for, because it splits the disease into two biologies with different epidemiology, genetics, and prognosis.[1]

By anatomical site: the antrum and pylorus (distal) is the commonest site worldwide and the one most tied to H. pylori, and its incidence is falling globally. The cardia and proximal stomach is rising fast in the West on the back of obesity and reflux, and behaves like a distal oesophageal adenocarcinoma. The body is the intermediate site; diffuse involvement of the whole stomach is the signature of linitis plastica.[1]

By depth of invasion: early gastric cancer (EGC) is confined to mucosa or submucosa regardless of nodes, carries a cure rate above 90 per cent, and is the target of screening and of endoscopic submucosal dissection. Advanced gastric cancer breaches muscularis propria and carries a far poorer outlook. Japan adds the Borrmann macroscopic types for advanced tumours — I polypoid, II ulcerating with raised edges, III ulcerating with infiltration, IV diffusely infiltrating (linitis plastica).[1]

By TNM (AJCC 8th edition):[1]

T is depth (T1 mucosa or submucosa, T2 muscularis propria, T3 subserosa, T4a serosa, T4b adjacent organs). N counts involved nodes (N1 one to two, N2 three to six, N3 seven or more) — which is exactly why an adequate lymphadenectomy (at least 16 nodes, ideally 25 or more) is needed both to stage and to cure. M1 is any distant metastasis, including non-regional nodes and peritoneal deposits.[1]

Geography, H. pylori, and the preventable cancer

Gastric cancer is the fifth commonest cancer and the fourth biggest cancer killer worldwide, with over a million new cases a year and a case fatality still above 70 per cent globally. Two facts make its epidemiology reward the candidate: a dramatic geographic gradient and one dominant, modifiable cause.[1]

Geography is extreme. The highest rates are in East Asia (Japan, Korea, China), Eastern Europe, and the Andean region of South America — up to ten times the lowest. North America, Western Europe, much of Africa, and South Asia sit at the bottom. Men are affected about twice as often as women. Distal (non-cardia) tumours are declining worldwide; proximal/cardia tumours are rising in the West with obesity and reflux.[1]

Helicobacter pylori is the single most important risk factor and the reason this is now a largely preventable cancer. The WHO/IARC classifies it as a Group 1 (definite) human carcinogen. Only a minority of the colonised ever develop cancer, but eradication lowers the subsequent risk — the rationale for test-and-treat programmes in high-prevalence countries.[2]

The non-modifiable set: blood group A (a modest intestinal-type excess); a background of chronic atrophic gastritis, intestinal metaplasia, or pernicious anaemia (mucosa already on the Correa conveyor); prior partial gastrectomy, especially Billroth II, raising risk after 15 to 20 years; and the hereditary syndromes — above all hereditary diffuse gastric cancer (HDGC) from a germline CDH1 (E-cadherin) mutation (autosomal dominant, 70 to 80 per cent lifetime risk of diffuse gastric cancer plus lobular breast cancer), then Lynch syndrome (MLH1/MSH2), familial adenomatous polyposis, and the hamartomatous polyposes (Peutz-Jeghers, juvenile).[1]

The modifiable set: the diet that drives intestinal-type cancer is salted, smoked, and pickled (delivering N-nitroso compounds and salt that strips the mucosal barrier) with too little fresh fruit and vegetables (losing the vitamin C and beta-carotene antioxidant cover). Smoking roughly doubles the risk. Obesity tracks mainly with proximal/cardia tumours. Epstein-Barr virus marks a distinct, better-prognosis molecular subtype in about 8 to 10 per cent, and coal, metal, and rubber occupations add a small excess.[1][2]

The Correa cascade — forty years from H. pylori to adenocarcinoma

The pathogenesis splits cleanly along the Lauren line: the intestinal type is the endpoint of a long inflammatory cascade, the diffuse type is loss of cell adhesion. Examiners test both mechanisms.[1]

The intestinal cascade begins when H. pylori colonises the mucus layer. Its virulence factors amplify injury: BabA binds the Lewis blood-group antigen on epithelium; CagA is injected through a type IV secretion system, is phosphorylated, and disrupts host signalling to drive proliferation and resist apoptosis; VacA vacuolates cells and blunts immune killing; urease makes ammonia that neutralises luminal acid. Chronic neutrophilic and monocytic inflammation generates reactive oxygen and nitrogen species that damage DNA. As glands die, acid output falls, the milieu alkalises, and bacterial overgrowth produces N-nitroso compounds — driving atrophy, then intestinal metaplasia, then dysplasia, then carcinoma.[2]

The diffuse type bypasses the glandular cascade entirely. The defining event is loss of E-cadherin (CDH1), the transmembrane protein of the adherens junction. Without it the cells lose cohesion and polarity, become motile, and infiltrate singly as signet-ring cells swollen with intracellular mucin. Germline CDH1 drives the hereditary form; sporadic diffuse tumours lose E-cadherin by mutation, promoter hypermethylation, or cleavage. Diffuse infiltration of all layers is linitis plastica — thick, rigid, leather-bottle, with a shrunken lumen.[1]

Patterns of spread dictate the clinical and surgical approach.[1]

• Direct extension through the wall to pancreas, transverse colon and mesocolon, spleen, left lobe of liver, and diaphragm.
• Lymphatic spread tracks the perigastric then the named arterial chains — left gastric, common hepatic, splenic, coeliac, hepatoduodenal, and para-aortic. The eponymous terminus is Virchow's node (left supraclavicular, reached via the thoracic duct); its palpability is Troisier's sign.
• Haematogenous spread seeds the liver (commonest solid organ) and the lungs; bone and brain are later.
• Transcoelomic spread gives peritoneal carcinomatosis with ascites, the Krukenberg tumour (bilateral ovarian, classically signet-ring, reached retrogradely), the Sister Mary Joseph nodule (umbilical deposit along the ligamentum teres), and Blumer's shelf (an anterior rectal-wall mass from a pelvic deposit).[1]

The trap of "just dyspepsia"

The hallmark of gastric cancer is delay. Early disease is silent or mimics functional dyspepsia; the textbook "cancer symptoms" appear only with advanced local disease or metastases. This is the section the examiner probes hardest.[1]

Everyone reaches for a PPI and reassures the patient. That is how you get a stage-IV stomach. New dyspepsia in anyone over 55, or dyspepsia with any alarm feature at any age, is cancer until the scope says otherwise.[1]

Early disease is often asymptomatic — found by screening in endemic regions — or produces vague postprandial fullness, bloating, or dyspepsia indistinguishable from benign ulcer disease.[1]

Symptoms of established disease reflect site, obstruction, and systemic effect:[1]

• Weight loss — the commonest presentation (over 60 per cent), often marked.
• Epigastric pain — vague, non-specific, classically unrelieved by food or antacids.
• Early satiety — a small-meal sensation, especially marked in linitis plastica, where the stomach is rigid.
• Dysphagia — localises the tumour to the cardia or gastro-oesophageal junction.
• Nausea and vomiting — points to a distal or antral tumour causing outlet obstruction; vomitus may hold undigested food.
• Anaemia — chronic occult blood loss (iron deficiency), or B12 deficiency after total gastrectomy or in pernicious anaemia.
• Haematemesis or melaena — tumour erosion; massive bleeding is an emergency.[1]

The eponymous metastatic signs are the pearls the examiner loves — and the ones juniors forget to look for:[1]

• Virchow's node (Troisier's sign) — a palpable left supraclavicular node, the sentinel of abdominal malignancy via the thoracic duct.
• Sister Mary Joseph nodule — a firm metastatic deposit at the umbilicus.
• Krukenberg tumour — a bilateral ovarian metastasis, classically signet-ring, in a woman with distension and a pelvic mass from an occult gastric primary.
• Blumer's shelf — a firm anterior rectal-wall mass on PR examination, from a pelvic peritoneal deposit.
• Ascites and an omentum-cake from peritoneal carcinomatosis.
• Hepatomegaly — a hard, nodular edge from liver metastases.
• An epigastric mass — the primary itself, fixed and irregular when advanced.[1]

The classic trap: the patient with weight loss and a left supraclavicular node sent home as "lymphadenitis." Virchow's node in this context is metastatic gastric cancer until proven otherwise — palpate the left supraclavicular fossa in every patient with epigastric symptoms or unexplained weight loss.[1]

Paraneoplastic phenomena are rare but examinable: acanthosis nigricans (velvety hyperpigmentation in flexures), the sign of Leser-Trélat (a sudden crop of seborrhoeic keratoses), Trousseau's syndrome (migratory venous thrombophlebitis), and polymyositis (a proximal myopathy with raised creatine kinase and the anti-Mi2 antibody).[1]

Atypical presentations to expect on call: the pernicious-anaemia patient with new dyspepsia; the young woman with abdominal distension harbouring a Krukenberg from an occult primary; iron-deficiency anaemia in any man or postmenopausal woman demanding OGD and colonoscopy; and the CDH1 carrier who may carry an advanced diffuse cancer at a young age despite trivial symptoms.[1]

The mimics — and the one test that sorts them

A patient with epigastric symptoms and weight loss generates a short, focused differential, and OGD with biopsy settles almost all of it. Each mimic is distinguished by its pattern, its endoscopic appearance, and its histology.[1]

Palpate Virchow's node before you reach for the scope

Examination is often normal in early disease — which is exactly why alarm symptoms, not physical signs, trigger the endoscopy. A focused exam hunts the stigmata of advanced or metastatic disease.[1]

• General: pallor (anaemia), cachexia and wasting, jaundice (liver failure or replacement), and cervical lymphadenopathy — palpate the left supraclavicular fossa for Virchow's node first.
• Abdomen: inspect for distension (ascites); palpate for a hard, irregular, fixed epigastric mass, hepatomegaly, a palpable omentum-cake, and shifting dullness or a fluid thrill.
• Digital rectal examination: feel the anterior rectal wall for Blumer's shelf.
• Umbilicus and skin: inspect for a Sister Mary Joseph nodule, acanthosis nigricans, or a sudden crop of seborrhoeic keratoses (sign of Leser-Trélat).[1]

[1]

The mantra for the whole topic, and the line that earns the mark: dyspepsia over fifty-five is cancer until the scope says otherwise.[1]

OGD diagnoses, CT and laparoscopy stage

Investigation has two jobs — make the diagnosis, then stage it accurately — because operability and the choice of perioperative therapy hinge on T, N, and M.[1]

Diagnostic — OGD with biopsy is the gold standard. It visualises the tumour, maps its site, size, and macroscopic morphology (ulcerative, polypoid, infiltrative), and takes tissue. Because gastric cancers can be submucosal and rimmed by inflammation or necrosis, take a minimum of six to eight biopsies from edge and base — the edge holds viable tumour, the base often only necrosis. For a flat early lesion, chromoendoscopy (indigo carmine) or narrow-band imaging highlights the abnormal pattern.[1]

Locoregional staging — endoscopic ultrasound (EUS) measures depth of wall invasion (T stage) and perigastric nodes, and matters most for deciding whether an early lesion suits endoscopic resection or for sizing a GOJ tumour before oesophagogastrectomy.[1]

Distant staging — CT chest, abdomen, and pelvis with IV contrast is the backbone (local invasion, nodes, liver and lung metastases). PET-CT is more sensitive for nodal and soft-tissue disease but unreliable for diffuse, mucinous, or signet-ring histology. The non-negotiable step is staging laparoscopy — CT misses peritoneal disease in 10 to 30 per cent of patients deemed resectable.[1]

Consultant confession: I do not book a curative gastrectomy without a staging laparoscopy first. CT is honest about the liver and lies about the peritoneum in roughly a quarter of patients — and a positive peritoneal washing upstages the patient to M1 and converts a curative operation into a palliative one before anyone picks up a scalpel.[1]

Staging laparoscopy inspects the peritoneum, gastric surface, and liver directly, and takes peritoneal washings for cytology; positive cytology is M1 and flips management from curative to palliative.[1]

Pre-operative bloods: full blood count (anaemia), iron studies, liver function tests (metastases), renal function and electrolytes, coagulation, and a group and save.[1]

Tumour markers — CEA, CA 19-9, and CA 72-4 — may be raised but lack sensitivity and specificity for diagnosis; they earn their place in monitoring response and detecting recurrence.[1]

Molecular testing is now standard staging in advanced disease and gates every targeted and immunotherapy option: HER2 by immunohistochemistry and in-situ hybridisation (overexpressed or amplified in 15 to 20 per cent — the gatekeeper for trastuzumab); MSI or mismatch-repair (MMR) status and PD-L1 combined positive score (for pembrolizumab or nivolumab); and EBV status.[7][8]

Management — Resuscitation

A gastric cancer may declare itself acutely — as outlet obstruction, upper GI bleeding, or perforation — and each is a surgical emergency handled in its own right before any cancer plan.[1]

Gastric outlet obstruction (distal tumour) presents with persistent vomiting of undigested food, dehydration, and a hypokalaemic, hypochloraemic metabolic alkalosis from gastric acid loss. Resuscitate with intravenous fluids (normal saline with potassium chloride correction), decompress with a wide-bore nasogastric tube, start a proton-pump inhibitor, and correct electrolytes before planning definitive surgery or a palliative bypass or stent.[1]

Acute upper GI bleeding (haematemesis or melaena from tumour erosion) is managed by the ABCDE approach: two large-bore cannulae, crystalloid resuscitation, crossmatch four units, transfuse to haemoglobin 70 g/L or above (80 g/L or above in cardiovascular disease), then urgent OGD for adrenaline injection plus thermal coagulation or clips, with a high-dose intravenous proton-pump inhibitor infusion. If uncontrolled, escalate to interventional radiology (embolisation) or emergency surgery — usually a life-saving limited procedure, not a cancer resection.[1]

Perforation of a gastric tumour is rare and catastrophic — sudden severe epigastric pain, peritonism, and free gas on an erect chest X-ray or CT. It needs emergency laparotomy, and in advanced disease the operation is usually palliative (biopsy and closure or limited resection), because a perforated tumour generally means advanced, incurable disease.[1]

Surgery is the only cure — D2, FLOT, and the Siewert fork

Surgery is the only curative treatment for localised gastric cancer, integrated with perioperative chemotherapy in the West and adjuvant therapy in Asia; for metastatic disease, treatment is palliative and increasingly personalised by molecular profile.[1][4]

Surgery

Extent of gastrectomy follows tumour site and the demand for a microscopically clear (R0) margin.[3][4]

• Distal (antrum, pylorus): distal (subtotal) gastrectomy removing about two-thirds of the stomach with a 5 to 6 cm distal margin, reconstructed by Billroth I or, more often, Roux-en-Y gastrojejunostomy (which diverts bile away from the remnant and cuts bile-reflux gastritis).
• Proximal (cardia, fundus): proximal (subtotal) gastrectomy or total gastrectomy, by the distal margin achievable.
• Body and diffuse tumours: total gastrectomy with a Roux-en-Y oesophagojejunostomy.
• Linitis plastica: total gastrectomy if resectable, but often irresectable at presentation and palliative.[1]

Lymphadenectomy is where the surgical controversy — and the exam question — lives.[3]

• D1 dissection removes only the perigastric nodes (stations 1 to 6) — lower morbidity, higher locoregional recurrence.
• D2 dissection adds the nodes along the left gastric, common hepatic, splenic, and coeliac arteries and the hepatoduodenal ligament (stations 7 to 12) — the standard of care in East Asia and increasingly the West.[1]

The Dutch D1D2 trial settled this. Early on, D2 carried higher postoperative mortality because the original protocol mandated routine splenectomy and distal pancreatectomy; the modern spleen-preserving, pancreas-sparing D2 avoids that excess. At 15 years, D2 delivered lower gastric-cancer-related death (35 per cent versus 48 per cent D1) and lower locoregional recurrence (12 per cent versus 22 per cent). Routine splenectomy and distal pancreatectomy are not recommended in a modern D2 unless the tumour directly invades those organs.[3]

Oesophagogastrectomy (thoracic or transhiatal) is reserved for GOJ tumours, classified by the Siewert system — type I distal oesophageal, type II true cardia, type III subcardial gastric — which decides an oesophageal versus gastric strategy.[1]

Endoscopic resection can be curative — but only for early gastric cancer meeting strict criteria. Endoscopic submucosal dissection (ESD) (or endoscopic mucosal resection for very small lesions) is potentially curative for differentiated histology, confined to the mucosa, two centimetres or less, and without ulceration — negligible nodal metastasis, en-bloc removal, no gastrectomy.[4]

Perioperative and adjuvant therapy

Three landmark strategies defined modern multimodal treatment, and each is examinable.[1]

[5] [6]

• Perioperative chemotherapy (MAGIC, then FLOT4). MAGIC established that perioperative ECF (epirubicin, cisplatin, 5-FU) — three preoperative and three postoperative cycles — lifted five-year survival from 23 to 36 per cent. FLOT4 then showed FLOT (5-FU, leucovorin, oxaliplatin, docetaxel) beats ECF/ECX, so perioperative FLOT is now the preferred regimen for resectable locally advanced gastric and GOJ adenocarcinoma in the West.[5]
• Adjuvant chemoradiotherapy (US, INT-0116). Where neoadjuvant chemotherapy is not given, postoperative 5-FU/leucovorin plus radiotherapy improves survival — the strategy that dominated US practice when D2 dissection was uncommon.[6]
• Adjuvant chemotherapy (Asia, ACTS-GC/CLASSIC). After a D2 gastrectomy, Asian practice gives adjuvant S-1 alone or capecitabine plus oxaliplatin (XELOX/CAPOX) for one year, reflecting the quality of D2 surgery in Japan and Korea.[4]

Metastatic and advanced disease

For unresectable or metastatic cancer, treatment is palliative — prolong survival and control symptoms — and is increasingly personalised by molecular profile.[1]

[7] [8]

• First-line palliative chemotherapy: a fluoropyrimidine plus platinum doublet — FOLFOX (5-FU, leucovorin, oxaliplatin) or CAPOX (capecitabine plus oxaliplatin) — often with a taxane as a triplet for fit patients.
• Trastuzumab (anti-HER2) is added to first-line chemotherapy for HER2-positive tumours (ToGA) — the first targeted therapy to improve survival in this disease.[7]
• Immunotherapy: nivolumab plus chemotherapy is now first-line for PD-L1-positive advanced disease (CheckMate 649), and pembrolizumab is reserved for MSI-H or dMMR tumours, which are uniquely checkpoint-responsive.
• Second-line options: ramucirumab (anti-VEGFR2), alone or with paclitaxel, and paclitaxel.
• Palliative procedures: self-expanding metal stenting for GOJ or outlet obstruction; surgical bypass or feeding jejunostomy/gastrostomy where stenting fails; radiotherapy for a bleeding tumour or painful metastasis; and paracentesis for symptomatic ascites.[8]

Subtypes that change the management question

Each subtype carries a distinct management question, and each is examinable.[1][4]

• Early gastric cancer (EGC) — mucosa or submucosa regardless of nodes. Lesions meeting the absolute criteria (differentiated, mucosal, two centimetres or less, no ulceration) are cured by endoscopic submucosal dissection; anything beyond needs surgical gastrectomy with D1-plus or D2. Five-year survival above 90 per cent is the entire rationale for screening.
• Linitis plastica — diffuse infiltrating signet-ring carcinoma turning the stomach into a rigid, non-distensible "leather bottle." Endoscopy can be deceptively normal (mucosa intact, disease submucosal), so biopsies are often negative and diagnosis may need EUS with deeper biopsies or CT. Prognosis is poor; total gastrectomy if resectable, but many cases are palliative.
• Hereditary diffuse gastric cancer (HDGC, CDH1) — autosomal dominant, with a 70 to 80 per cent lifetime risk of diffuse gastric cancer plus lobular breast cancer. After counselling, prophylactic total gastrectomy is recommended, typically between ages 18 and 40, because surveillance endoscopy misses the multifocal submucosal signet-ring foci.
• Gastric MALT lymphoma — not an adenocarcinoma but a vital differential, tied to H. pylori. Low-grade MALT often regresses completely after H. pylori eradication; the t(11;18) translocation predicts non-response and a need for chemoimmunotherapy or radiotherapy.
• Gastrointestinal stromal tumour (GIST) — a submucosal spindle-cell tumour driven by KIT or PDGFRA mutations, CD117 (c-KIT) positive. Localised disease is resected; unresectable or metastatic disease responds dramatically to imatinib.
• Gastric neuroendocrine tumours — type I (autoimmune chronic atrophic gastritis, indolent), type II (Zollinger-Ellison or MEN1), type III (sporadic, aggressive); management varies by type and grade.[1]

[1]

Complications & pitfalls

Complications split into disease-related and treatment-related, and the post-gastrectomy complications are among the most tested in general surgery.[1]

Disease-related: outlet obstruction (distal), upper GI bleeding, perforation (rare, catastrophic), fistulation into colon or pancreas, and the metastatic burden — liver (commonest solid organ), peritoneum (ascites, Krukenberg, Blumer's shelf), lung, bone, brain.[1]

Surgical complications after gastrectomy:[1]

• Anastomotic leak — the oesophagojejunal join after total gastrectomy is the highest-risk join. Presents around days 5 to 7 with fever, abdominal or pleuritic pain, and tachycardia, and may progress to sepsis. A water-soluble contrast swallow or CT confirms it; management runs from nil-by-mouth, drainage, and parenteral nutrition for a contained leak to stenting or re-operation for a free leak.
• Dumping syndrome — the price of losing the pylorus and the gastric reservoir. Early dumping (15 to 30 minutes post-meal): hyperosmolar contents rush into the small bowel, drawing fluid into the lumen — palpitations, flushing, dizziness, diarrhoea, cramping. Late dumping (1 to 3 hours): exaggerated insulin release gives reactive hypoglycaemia. Management is dietary — small, frequent, low-carbohydrate, dry meals (fluids between meals), with octreotide for refractory cases.
• Bile-reflux (alkaline) gastritis — bile in the stomach or oesophagus; nausea, pain, bilious vomiting. A Roux-en-Y reconstruction minimises it.
• Postgastrectomy nutritional deficiency — after total gastrectomy the patient loses intrinsic factor and needs lifelong intramuscular vitamin B12; iron, calcium, folate, and fat-soluble vitamins also commonly fall (less acid, rapid transit), mandating supplementation and monitoring.
• Afferent-loop syndrome, postvagotomy diarrhoea, small-bowel obstruction, and incisional hernia round out the longer-term mechanical complications.[1]

Classic management pitfalls — every one of these fails a patient:[1]

• No OGD in the over-55 with new dyspepsia (the recurring trainee error).
• Weight loss put down to "age" or "depression" without investigation.
• Virchow's node missed on neck examination.
• Staging laparoscopy omitted before curative surgery — and occult peritoneal disease found at laparotomy.
• HER2 and PD-L1 or MSI not tested in advanced disease — denying trastuzumab or immunotherapy.
• Lifelong B12 forgotten after total gastrectomy.[1]

Prognosis & disposition

Overall five-year survival is 20 to 30 per cent, almost entirely a function of late presentation — but stage for stage, gastric cancer is curable when caught early.[1]

Favourable: intestinal histology, early gastric cancer, distal location, an R0 (microscopically clear) resection, and fewer than four involved nodes. Unfavourable: diffuse and signet-ring histology, linitis plastica, proximal/cardia site, serosal penetration, peritoneal metastases, and raised tumour markers.[1]

Disposition and follow-up: after a curative resection, follow clinically with bloods (full blood count, liver function tests, B12) and CT as indicated — there is no single universal surveillance protocol. After total gastrectomy, lifelong intramuscular vitamin B12 is mandatory. Offer H. pylori eradication postoperatively to lower the risk of a metachronous cancer in the remnant.[1]

Special populations

• H. pylori eradication after resection is recommended for all post-resection patients to cut the risk of metachronous tumours in the remnant. Standard first-line is a triple regimen — a proton-pump inhibitor plus clarithromycin plus amoxicillin (or metronidazole) for 14 days; in areas of high clarithromycin resistance, a bismuth-based quadruple regimen is preferred.[2]

[1]

• CDH1 mutation carriers (hereditary diffuse gastric cancer). After genetic counselling and testing, prophylactic total gastrectomy is recommended between ages 18 and 40, with pre-operative counselling on the nutritional sequelae — dumping, weight loss, and lifelong B12 dependence.[1]
• Elderly and frail patients. For advanced disease, favour endoscopic stenting over surgery for obstruction, weigh the toxicity of neoadjuvant chemotherapy carefully, and adopt a palliative approach with early specialist-nurse and dietetic input.
• Screening populations (Japan and Korea). National programmes of barium meal photofluorography and/or direct OGD from around age 40 detect early gastric cancer and explain the markedly better survival in East Asia. In low-incidence countries (UK, US, India) population screening is not cost-effective; instead, endoscopic surveillance targets high-risk groups — atrophic gastritis or intestinal metaplasia, pernicious anaemia, prior gastrectomy, or a family history of HDGC.[4]

Evidence, guidelines & regional differences

The evidence base for gastric cancer is unusually mature, and four landmark trials define modern practice; regional differences arise from incidence, screening, and surgical tradition.[1][3]

The Dutch D1D2 trial settled the lymphadenectomy debate: although early D2 mortality was inflated by routine splenectomy and distal pancreatectomy, the modern spleen-preserving D2 delivers lower cancer-related death and recurrence at 15 years and is the global oncological standard.[3] MAGIC brought perioperative chemotherapy to the West,[5] refined by FLOT4 to the docetaxel-based FLOT regimen now preferred. INT-0116 underpins the US adjuvant chemoradiotherapy strategy used when neoadjuvant chemotherapy is not given.[6] In advanced disease, ToGA made HER2 testing mandatory and trastuzumab standard for HER2-positive tumours,[7] while CheckMate 649 brought immunotherapy into the first line for PD-L1-positive disease.[8]

[4]

Exam pearls

• Correa cascade: normal mucosa, then chronic gastritis (H. pylori), then atrophic gastritis, then intestinal metaplasia, then dysplasia, then adenocarcinoma — over decades.[2]
• H. pylori is a WHO Class I carcinogen — the single most important risk factor; eradication reduces cancer risk.[2]
• Lauren classification: intestinal type (gland-forming, H. pylori-linked, older males, distal stomach, better prognosis) versus diffuse type (signet-ring, CDH1 loss, linitis plastica, younger, worse prognosis).[1]
• Eponymous metastatic signs: Virchow's node (left supraclavicular, Troisier's sign), Sister Mary Joseph nodule (umbilicus), Krukenberg (ovary), Blumer's shelf (rectal shelf), acanthosis nigricans or sign of Leser-Trélat (paraneoplastic).[1]
• D2 lymphadenectomy is the standard for curative gastrectomy (Dutch D1D2 15-year follow-up); routine splenectomy and distal pancreatectomy are not done.[3]
• Perioperative FLOT for resectable locally advanced disease (MAGIC then FLOT4). Adjuvant chemoradiotherapy (INT-0116) where neoadjuvant chemo not given.[5][6]
• HER2-positive metastatic disease gets trastuzumab (ToGA); PD-L1-positive or MSI-H gets nivolumab or pembrolizumab (CheckMate 649).[7][8]
• Lifelong intramuscular B12 after total gastrectomy (loss of intrinsic factor).[1]
• Dysphagia equals urgent OGD; new dyspepsia over 55 equals urgent OGD (NICE NG12).[1]
• CDH1 mutation equals hereditary diffuse gastric cancer equals prophylactic total gastrectomy between ages 18 and 40.[1]
• Linitis plastica equals "leather bottle" stomach equals diffuse signet-ring carcinoma; endoscopy may look deceptively normal.
• Early gastric cancer (mucosa or submucosa regardless of nodes) is curable by endoscopic submucosal dissection if it meets strict criteria.[4]

Ward-round test

Stem 1 — the CDH1 carrier at thirty (answer)

A 30-year-old woman whose mother died of diffuse gastric cancer at 40 tests positive for a germline CDH1 mutation. Surveillance OGD with multiple random biopsies is normal. What is the recommended management, and why does a normal scope not reassure you? Model: This is hereditary diffuse gastric cancer (HDGC) — autosomal dominant, with a 70 to 80 per cent lifetime risk of diffuse gastric cancer. The recommended management is prophylactic total gastrectomy, typically between ages 18 and 40, because the foci are multifocal and submucosal and surveillance endoscopy routinely misses them — a normal scope does not exclude disease. Counsel pre-operatively on dumping, weight loss, and lifelong intramuscular B12.[1]

Stem 2 — new dyspepsia at fifty-eight with weight loss (answer)

A 58-year-old man has three months of new epigastric fullness and 6 kg of weight loss. What is the first investigation, and what thresholds drove the referral? Model: The first investigation is urgent OGD (upper gastrointestinal endoscopy) with biopsy — the NICE NG12 2-week-wait applies twice over: new-onset dyspepsia in a patient aged 55 or over, and dyspepsia with an alarm feature (weight loss) at any age, both mandate urgent endoscopy to exclude gastric cancer. Stage any confirmed cancer with CT chest/abdomen/pelvis, EUS for depth, and staging laparoscopy before any curative surgery, because CT misses peritoneal disease in 10 to 30 per cent of apparently resectable patients. The mantra holds: dyspepsia over fifty-five is cancer until the scope says otherwise.[1]

Exam application bank (NEET-PG / INICET)

One-line answer

Gastric carcinoma is an adenocarcinoma of the gastric epithelium and the fifth commonest cancer worldwide. Helicobacter pylori (a WHO Class I carcinogen) drives most intestinal-type tumours along the Correa cascade over decades, while CDH1 loss drives the diffuse type and linitis plastica. Presentation is late — epigastric pain, weight loss, early satiety, dysphagia (proximal), vomiting (distal), anaemia — with eponymous metastatic signs (Virchow's node, Sister Mary Joseph, Krukenberg, Blumer's shelf). Diagnose by OGD and biopsy; stage with CT plus EUS plus staging laparoscopy. Cure is gastrectomy with D2 lymphadenectomy plus perioperative FLOT for resectable locally advanced disease; trastuzumab for HER2-positive and nivolumab for PD-L1-positive or MSI-H metastatic disease.[1]

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose or route if drug therapy is standard. [1]

Stem 2 — Unstable or complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes. [1]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change. [1]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each. [1]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU, ICU, or theatre, and what follow-up is mandatory. [1]

Rapid viva checklist

1. Definition plus classification
2. Pathophysiology chain
3. Bedside signs and criteria
4. Score with exact components (if any)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline or trial name if classic
10. Three exam traps

[1]

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Gastric Carcinoma.[1]

References

1. [1]Sundar R, Nakayama I, Markar SR, et al. Gastric cancer Lancet, 2025.PMID 40319897
2. [2]Duan Y, Xu Y, Dou Y, et al. Helicobacter pylori and gastric cancer: mechanisms and new perspectives J Hematol Oncol, 2025.PMID 39849657
3. [3]Songun I, Putter H, Kranenbarg EM, et al. Surgical treatment of gastric cancer: 15-year follow-up results of the randomised nationwide Dutch D1D2 trial Lancet Oncol, 2010.PMID 20409751
4. [4]Shen L, Shan YS, Hu HM, et al. Management of gastric cancer in Asia: resource-stratified guidelines Lancet Oncol, 2013.PMID 24176572
5. [5]Cunningham D, Allum WH, Stenning SP, et al. Perioperative chemotherapy versus surgery alone for resectable gastroesophageal cancer N Engl J Med, 2006.PMID 16822992
6. [6]Macdonald JS, Smalley SR, Benedetti J, et al. Chemoradiotherapy after surgery compared with surgery alone for adenocarcinoma of the stomach or gastroesophageal junction N Engl J Med, 2001.PMID 11547741
7. [7]Bang YJ, Van Cutsem E, Feyereislova A, et al. Trastuzumab in combination with chemotherapy versus chemotherapy alone for treatment of HER2-positive advanced gastric or gastro-oesophageal junction cancer (ToGA): a phase 3, open-label, randomised controlled trial Lancet, 2010.PMID 20728210
8. [8]Janjigian YY, Shitara K, Moehler M, et al. First-line nivolumab plus chemotherapy versus chemotherapy alone for advanced gastric, gastro-oesophageal junction, and oesophageal adenocarcinoma (CheckMate 649): a randomised, open-label, phase 3 trial Lancet, 2021.PMID 34102137