The stomach is part of the digestive system, located between the oesophagus and the small intestine. It secretes enzymes and gastric acid to aid in food digestion, as well as the intrinsic factor necessary for absorption of vitamin B12, and acts as a receptacle for masticated food, which is sent to the small intestines though muscular contractions. The body of the stomach is lined with a mucous membrane consisting of columnar epithelial cells and glands, surrounded by muscle.
Incidence and survival rates
Stomach cancer – also known as gastric cancer – is the fifth most common cancer worldwide. Around 952,000 new cases of stomach cancer were recorded globally in 2012, accounting for seven per cent of all new cases of cancer.
Men are twice as likely as women to develop stomach cancer, and it is more common in older adults over the age of 50. For example, the average age at diagnosis in the US is 72 years.
Stomach cancer is the third most common cause of death from cancer. Symptoms often only appear at a late stage, which contributes to a poor prognosis. For example, in Europe and the US the five-year survival rate of stomach cancer is about 25 to 28 per cent, increasing to about 63 per cent if the cancer is diagnosed at an early stage. However, these survival rates are worse in less developed countries where stomach cancer is typically detected at a more advanced stage.
About 70 per cent of cases of stomach cancer occur in less developed countries with about half of all cases in Eastern Asia, particularly China.
Globally, overall incidence rates of stomach cancer are declining. This is attributed to a decrease in Helicobacter pylori infection and the use of refrigeration to preserve foods rather than using salt. Stomach cancer is classified into different types according to location of the tumour. Stomach cardia cancer occurs at the top part of the stomach closest to the oesophagus, and stomach non-cardia cancer occurs in all other areas of the stomach.
Stomach non-cardia cancer is more common than stomach cardia cancer, globally, and is most prevalent in Asia. Rates of stomach non-cardia cancer are declining. Stomach cardia cancer is more common than non-cardia cancer in more developed countries such as the UK and US, and is increasing in all countries.
The cancer statistics quoted in the Third Expert Report are from the GLOBOCAN 2012 database. The International Agency for Research on Cancer (IARC) updated these statistics in September 2018, after the publication of the Third Expert Report. Find the latest stomach cancer statistics.
Lifestyle factors and stomach cancer risk
In this report from our Continuous Update Project (CUP) – the world’s largest source of scientific research on cancer prevention and survivorship through diet, nutrition and physical activity – we analyse global research on how certain lifestyle factors affect the risk of developing stomach cancer. This webpage forms part of the World Cancer Research Fund/American Institute for Cancer Research Third Expert Report Diet, Nutrition, Physical Activity and Cancer: a Global Perspective.
Findings on stomach cancer
There is strong evidence that:
- consuming alcoholic drinks INCREASES the risk of stomach cancer
- consuming salt-preserved foods INCREASES the risk of stomach cancer
- being overweight or obese INCREASES the risk of stomach cardia cancer
There is some evidence that:
- consumption of grilled or barbecued meat and fish might increase the risk of stomach cancer
- consumption of processed meat might increase the risk of stomach non-cardia cancer
- consuming little or no fruit might increase the risk of stomach cancer
- consumption of citrus fruit might decrease the risk of stomach cardia cancer
Other causes of stomach cancer
In addition to the findings on diet, nutrition and physical activity outlined above, other established causes of stomach cancer include:
Smoking is a cause of stomach cancer. It is estimated that 11 per cent of cases worldwide are attributable to tobacco use.
Helicobacter pylori infection is a cause of stomach non-cardia cancer. Also, infection with Epstein-Barr virus is under investigation as a contributor to stomach cancer.
- industrial chemical exposure
Occupational exposure to dusty and high-temperature environments – such as woodprocessing and food-machine operators – has been associated with an increased risk of stomach cancer. Other industries including rubber manufacturing, coal mining, metal processing and chromium production have also been associated with an elevated risk of this cancer.
The lining of the stomach is exposed to carcinogens present in foods, which are held in the stomach for a period of up to five hours during digestion.
More than 95 per cent of stomach cancers are adenocarcinomas, with primary gastric lymphoma being the second most common malignancy. Pathogenesis and aetiology differ between cardia and non-cardia cancers.
Chronic gastritis, inflammation brought about by a variety of environmental factors and ageing can eventually lead to changes in the characteristics of the stomach mucosal cells. These changes appear to be precursor conditions to the development of non-cardia cancer.
Non-cardia cancers may be either intestinal (well-differentiated) or diffuse (undifferentiated, from mucus-producing cells). Intestinal types commonly undergo a cascade from normal mucosa through chronic gastritis to atrophic gastritis, intestinal dysplasia, and then adenocarcinoma. This progression may take several years. Intestinal types are more common in males and older adults, whereas diffuse types may occur in all age groups with equal sex distribution and show more rapid progression and poorer prognosis.
H. pylori infection is strongly implicated in the aetiology of intestinal non-cardia cancer. Infection appears to interact with dietary factors. One pooled analysis reported an increased stomach cancer risk with H. pylori infection (RR = 2.9), increasing to RR = 5.9 when the analysis was restricted to cases occurring at least 10 years after infection diagnosis. A rare, genetically inherited form of diffuse stomach cancer also exists, which is unrelated to H. pylori infection. Rare hereditary variants contribute to about 1–3 per cent of stomach cancers.
The pathogenesis of cardia cancer is less well established, although it is associated with inflammation of the cardia. There are similarities between cardia cancer and oesophageal adenocarcinoma, which is inversely associated with H. pylori infection and positively with Barrett’s oesophagus. However, evidence for Barrett’s oesophagus as a causal factor in cardia cancer is not conclusive. Cardia cancer may, in some populations, be inversely associated with H. pylori infection, but cardia cancer in the presence of H. pylori infection shows an association with gastric atrophy. A dual aetiology, with some tumours linked to H. pylori infection and some to reflux injury, is emerging.
Inherited mutations of certain genes, particularly the GSTM1-null phenotype, are associated with elevated risk of stomach cancer. Certain polymorphisms of interleukin genes (IL-17 and IL-10) have also been associated with increased risk of stomach cancer, particularly in Asian populations. These polymorphisms may interact with H. pylori infection and smoking to affect cancer risk.
Full references and a summary of the mechanisms underpinning all the findings can be found in the stomach cancer report.
How the research was conducted
The global scientific research on diet, nutrition, physical activity and the risk of stomach cancer was systematically gathered and analysed, and then independently assessed by a panel of leading international scientists in order to draw conclusions about which of these factors increase or decrease the risk of developing this cancer.
Published findings in peer-reviewed journals
Selected findings from this report have been published in peer-reviewed journals. Details of the papers and links to the abstract in PubMed are below:
An update of the WCRF/AICR systematic literature review and meta-analysis on dietary and anthropometric factors and esophageal cancer risk. S Vingeliene, DSM Chan, AR Vieira, E Polemiti, C Stevens, L Abar, D Navarro Rosenblatt, DC Greenwood, T Norat. Ann Oncol. 2017 Oct 1;28(10):2409-2419. Abstract