What Causes Stomach Cancer?

There are many known risk factors for stomach cancer, but it is not known exactly how these factors cause cells of the stomach lining to become cancerous. This is the subject of ongoing research.

Several changes thought to be pre-cancerous can occur in the stomach lining.

In chronic atrophic gastritis, the normal glands of the stomach are either decreased or absent. There is also some degree of inflammation (the stomach cells are damaged by cells of the immune system). Atrophic gastritis is often caused by H pylori infection. It can also be caused by an autoimmune reaction, in which a person’s immune system attacks the cells lining the stomach. Some people with this condition go on to develop pernicious anemia or other stomach problems, including cancer. It is not known exactly how this condition might progress to cancer.

Another possible pre-cancerous change is intestinal metaplasia. In this condition, the normal lining of the stomach is replaced with cells that closely resemble the cells that usually line the intestine. People with this condition usually have chronic atrophic gastritis as well. How and why this change occurs and progresses to stomach cancer is not well understood. This might also be related to H pylori infection.

Recent research has provided clues on how some stomach cancers form. For instance, H pylori bacteria, particularly certain subtypes, can convert substances in some foods into chemicals that cause mutations (changes) in the DNA of the cells in the stomach lining. This may also explain why certain foods such as preserved meats increase a person’s risk for stomach cancer. On the other hand, some of the foods that might lower stomach cancer risk, such as fruits and vegetables, contain antioxidants that can block substances that damage a cell’s DNA.

Scientists have made a lot of progress in understanding how certain changes in DNA can cause normal stomach cells to grow abnormally and form cancers. DNA is the chemical in cells that carries our genes, which control how our cells function. We look like our parents because they are the source of our DNA. But DNA affects more than how we look.

Some genes control when cells grow and divide into new cells:

  • Genes that help cells grow and divide are called oncogenes.
  • Genes that help keep cell division under control or cause cells to die at the right time are called tumor suppressor genes.

DNA changes that turn on oncogenes or turn off tumor suppressor genes can cause cancers.

Inherited mutations (abnormal changes) in some genes (as explained in Stomach Cancer Risk Factors ) can increase a person’s stomach cancer risk. These are thought to cause only a small percentage of stomach cancers. Still, genetic testing can be done to look for the gene mutations that can cause some inherited cancer syndromes. You can read more in Genetics and Cancer.

Most of the gene changes that lead to stomach cancer occur after birth. Some of these changes might be caused by risk factors such as H pylori infection or tobacco use. But other gene changes may just be random events that sometimes happen inside cells, without having an outside cause.

The American Cancer Society medical and editorial content team

Our team is made up of doctors and oncology certified nurses with deep knowledge of cancer care as well as journalists, editors, and translators with extensive experience in medical writing.

Avital I, Stojadinovic A, Pisters PWT, Kelsen DP, Willett CG. Cancer of the stomach, In: DeVita VT, Lawrence TS, Rosenberg SA, eds. DeVita, Hellman, and Rosenberg’s Cancer: Principles and Practice of Oncology. 10th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2015.

Gunderson LL, Donohue JH, Alberts SR, Ashman JB, Jaroszewski DE. Cancer of the Stomach and Gastroesophageal Junction. In: Niederhuber, JE, Armitage, JO, Doroshow, JH, Kastan, MB, Tepper, JE, eds. In Abeloff’s
Clinical Oncology.
5th ed. Philadelphia, Pa: Elsevier; 2014:1240-1270.

Last Revised: December 14, 2017

American Cancer Society medical information is copyrighted material. For reprint requests, please see our Content Usage Policy.