Stomach cancer (gastric cancer)
Stomach cancer remains one of the commoner causes of cancer death worldwide, though its incidence has fallen substantially over several decades. Its central difficulty is that it produces no symptoms until it is reasonably advanced, and the symptoms it then produces — indigestion, fullness, nausea — are the commonest symptoms in general practice. The result is that in countries without screening programmes, most cases are diagnosed at a stage where cure is harder. In Japan and Korea, where screening endoscopy is routine, the majority are found early and the survival figures are entirely different. That contrast is the strongest argument for investigating persistent upper abdominal symptoms rather than treating them empirically for months.
How it forms
Most gastric cancers are adenocarcinomas, and the majority develop through a well-characterised sequence driven by chronic inflammation — the Correa cascade:
- Chronic gastritis, most often from Helicobacter pylori infection, or autoimmune.
- Atrophic gastritis — the specialised acid-producing glands are progressively destroyed and replaced by fibrous tissue. Acid output falls, which allows bacterial overgrowth and the generation of nitrosamines.
- Intestinal metaplasia — the stomach lining is replaced by cells resembling intestinal lining, an adaptation to the altered environment.
- Dysplasia — accumulating genetic damage produces cells that are architecturally and cytologically abnormal but still confined.
- Invasive adenocarcinoma.
This sequence takes decades, which is what makes eradication of H. pylori and endoscopic surveillance of the intermediate stages worthwhile. Eradicating the infection reduces the subsequent risk of gastric cancer, and does so most effectively when performed before atrophy is established.
The two histological types
The Laurén classification divides gastric cancer into two types that differ in cause, appearance and behaviour, and the distinction is practically useful.
- Intestinal type — forms glands, arises through the Correa cascade described above, occurs in older patients, is commoner in men, tends to be in the antrum, spreads to the liver via the portal vein, and is the type whose incidence has fallen with improved food preservation and declining H. pylori prevalence.
- Diffuse type — does not form glands. Individual cells with intracellular mucus pushing the nucleus to one side (signet ring cells) infiltrate the wall, provoking a dense fibrous reaction that thickens and stiffens the stomach without forming an obvious mass. When the whole stomach is involved it is called linitis plastica. It occurs in younger patients, affects men and women equally, is not strongly associated with the Correa sequence, spreads early to the peritoneum, and carries a worse prognosis. Loss of the cell adhesion molecule E-cadherin, encoded by CDH1, is the characteristic molecular event — the cells simply do not stick to one another, which is why they infiltrate diffusely.
The diffuse type is also the type that is most easily missed at endoscopy, because there may be no ulcer or mass to biopsy — only a rigid, poorly distensible stomach. Suspicion in that situation warrants deep or repeat biopsies.
Risk factors
- Helicobacter pylori — the single most important modifiable factor
- atrophic gastritis, intestinal metaplasia, pernicious anaemia
- diet high in salt, salted and smoked foods and nitrates; low in fresh fruit and vegetables
- smoking; alcohol
- previous partial gastrectomy, with bile reflux into the gastric remnant — risk rising after fifteen to twenty years
- obesity, particularly for junctional tumours
- Epstein-Barr virus, in a distinct molecular subgroup
- family history, and hereditary diffuse gastric cancer from germline CDH1 mutation, which carries a very high lifetime risk and for which prophylactic total gastrectomy is recommended — a major decision requiring specialist genetic counselling
- Lynch syndrome, familial adenomatous polyposis, Li-Fraumeni syndrome
Symptoms
Early gastric cancer is asymptomatic or causes only vague dyspepsia. Later features include:
- persistent indigestion or epigastric discomfort unresponsive to treatment
- weight loss and loss of appetite
- early satiety — particularly suggestive of diffuse disease, where the stomach cannot distend
- nausea and vomiting; vomiting of retained food if the outlet is obstructed
- dysphagia, with junctional tumours
- iron-deficiency anaemia, fatigue, or overt bleeding — vomiting blood or black stools
- a palpable epigastric mass
- signs of advanced disease: an enlarged left supraclavicular node (Virchow's node), a periumbilical nodule (Sister Mary Joseph nodule), ascites, jaundice
Alarm features requiring prompt endoscopy: weight loss, dysphagia, persistent vomiting, anaemia, gastrointestinal bleeding, a mass, or new dyspepsia in a patient over fifty-five. New persistent indigestion in an adult that does not resolve should be investigated, not treated indefinitely.
How the diagnosis is made
- Endoscopy with multiple biopsies — the diagnostic test. At least six to eight biopsies are taken from an ulcerated lesion. Where diffuse disease is suspected and superficial biopsies are negative, deeper or repeat biopsies are required rather than reassurance.
- CT of chest, abdomen and pelvis — local extent, nodal disease, liver and lung metastases.
- Endoscopic ultrasound — the most accurate assessment of depth of invasion and local nodes, particularly important in deciding whether early lesions can be treated endoscopically.
- Staging laparoscopy with peritoneal washings — important, and easily undervalued. It detects small-volume peritoneal disease invisible on CT in a meaningful proportion of patients, particularly with diffuse-type tumours, and spares them a futile gastrectomy. Positive cytology in the washings alone indicates disease beyond the reach of surgery.
- PET-CT in selected patients; it is less reliable in diffuse and mucinous tumours, which are often not avid.
- Biomarker testing — HER2, PD-L1, mismatch repair or microsatellite instability status, and Epstein-Barr virus, all of which determine eligibility for targeted and immune treatments.
Treatment
Planned by a specialist multidisciplinary team, and depending on stage, histological type, biomarkers and fitness.
Early gastric cancer
Tumours confined to the mucosa, well differentiated, without ulceration and within size criteria, carry a very low risk of lymph node involvement and can be cured by endoscopic submucosal dissection, which removes the lesion intact for complete pathological assessment. If the specimen shows deeper invasion, lymphovascular invasion or poor differentiation, gastrectomy follows.
Locally advanced, operable disease
Perioperative chemotherapy — given before and after surgery — is standard, and improves survival substantially compared with surgery alone. Chemoradiotherapy has a role in selected cases, particularly junctional tumours.
Surgery
The aim is complete resection with clear margins together with an adequate lymphadenectomy.
- Subtotal (distal) gastrectomy for antral and distal tumours, preserving the upper stomach — associated with better nutritional outcomes and preferred where an adequate margin can be achieved.
- Total gastrectomy for proximal, mid-body and diffuse tumours, with reconstruction usually by a Roux-en-Y oesophagojejunostomy.
- D2 lymphadenectomy — removal of the perigastric nodes together with those along the named arteries — is the standard of care, and improves disease-specific survival when performed by experienced surgeons with preservation of the spleen and pancreas.
- Minimally invasive and robotic gastrectomy gives equivalent oncological results with faster recovery in experienced hands.
As with oesophageal surgery, outcomes after gastrectomy are consistently better in high-volume specialist units, and it is reasonable for a patient to ask about this.
Advanced disease
Chemotherapy is the mainstay, with trastuzumab added for HER2-positive tumours and immunotherapy for those with high PD-L1 expression or mismatch repair deficiency, both of which have improved outcomes meaningfully. Palliative measures include stenting or bypass for obstruction, radiotherapy for bleeding, nutritional support and early palliative care involvement. Selected patients with limited peritoneal disease are treated in specialist centres with cytoreductive surgery and heated intraperitoneal chemotherapy, within defined criteria.
Recovery after gastrectomy
Hospital stay is typically seven to twelve days. Return to normal activity takes two to three months. Lasting changes are expected and should be explained beforehand rather than discovered afterwards:
- small, frequent meals — six or more a day — permanently after total gastrectomy
- weight loss of the order of ten to fifteen per cent, which then stabilises
- dumping syndrome — early dumping, within thirty minutes, from rapid delivery of concentrated food into the small bowel drawing fluid in, causing cramps, palpitations and diarrhoea; late dumping, one to three hours after eating, from a reactive drop in blood sugar. Both are managed by separating fluids from solids, avoiding concentrated sugars, and eating small frequent meals.
- Vitamin B12 deficiency is inevitable after total gastrectomy, since intrinsic factor is lost. Lifelong injections are required — this is not optional and is occasionally overlooked.
- iron and calcium deficiency, and reduced bone density over years, requiring monitoring and supplementation
- bile reflux, and diarrhoea in some patients
Specialist dietetic support is an essential part of the treatment, not an adjunct to it.
Follow-up
Regular review with attention to nutrition, weight, B12, iron and bone health, with imaging and endoscopy as indicated. Most recurrences occur within the first two to three years.
When to seek an opinion
Persistent indigestion lasting more than a few weeks, especially over the age of fifty-five or with any alarm feature; unexplained weight loss; iron-deficiency anaemia; early satiety; or a family history of gastric cancer, particularly diffuse-type or at a young age, which warrants genetic assessment.
Common questions
I have had indigestion for months. Should I be worried?
Most persistent indigestion is not cancer. But indigestion that does not settle with treatment, or that comes with weight loss, difficulty swallowing, vomiting, tiredness from anaemia or feeling full very quickly, should be investigated with an endoscopy rather than treated for longer. The test is quick, and the reassurance from a normal result is worth having.
Is stomach cancer caused by the bacterium I was told about?
Helicobacter pylori is the single most important known cause, acting over decades by causing long-standing inflammation of the lining. Most people who carry it never develop cancer. Treating it reduces the risk, and does so most effectively when treated before the lining has changed.
Will my whole stomach have to be removed?
Not always. If the tumour is in the lower part, the upper portion can often be preserved, which makes eating afterwards considerably easier. Removing the whole stomach is necessary for tumours higher up or of the type that spreads through the wall. Very early tumours can sometimes be removed through an endoscope with no surgery at all.
How will I eat without a stomach?
You will eat, in a different pattern. The gullet is joined directly to the small intestine, so there is no reservoir and meals must be small and frequent — six or more a day. Most people adapt over several months, lose some weight and then stabilise. A specialist dietitian works with you from before the operation onwards, and this support makes a substantial difference.
Why do I need chemotherapy before the operation?
Because treatment given first shrinks the tumour, making complete removal more likely, and treats cells that may already have spread but cannot yet be seen. It has been shown to improve survival compared with surgery alone, and it is generally better tolerated before a major operation than after one.
What are dumping symptoms?
After the stomach is removed or reduced, food passes rapidly into the intestine. Soon after eating this can cause cramps, sweating, palpitations and diarrhoea; an hour or two later it can cause shakiness from a drop in blood sugar. Both are common, both improve with time, and both respond well to eating small frequent meals, avoiding sugary food and drink, and taking fluids between rather than with meals.
Why do I need B12 injections for life?
Because the stomach makes the substance needed to absorb vitamin B12 from food, and without a stomach that absorption is not possible. Injections replace it directly. Without them, anaemia and nerve damage develop over a few years, so this is an important part of long-term care.
Does stomach cancer run in families?
The great majority of cases do not. A small proportion are due to an inherited fault, particularly a type that causes the diffuse form at a young age and also carries a raised risk of a particular type of breast cancer. Where there are several affected relatives, or a case at a young age, genetic assessment should be offered, because it changes what is recommended for the whole family.
Related conditions
Other conditions of the stomach covered on this site:
- Peptic ulcer disease
- Perforated and bleeding peptic ulcer
- Gastric outlet obstruction
- Gastric polyps
- Gastrointestinal stromal tumour (GIST)
- Gastric neuroendocrine tumours (gastric carcinoids)
This page provides general information and does not replace an individual medical consultation. Assessment and treatment are decided for each patient after review of their history, examination, investigations and discussion in a multidisciplinary meeting.