Helicobacter pylori, commonly known as H. pylori, is a bacterium that frequently inhabits the human stomach. This microorganism colonizes the stomach lining of approximately half the world’s population. Many individuals carrying H. pylori remain asymptomatic throughout their lives. The bacterium often establishes a lifelong presence within the host.
H. pylori’s Connection to Cancer
H. pylori is recognized as a biological carcinogen, meaning it can cause cancer. This bacterium is primarily linked to two types of stomach cancer: gastric adenocarcinoma, the most common form, and gastric mucosal-associated lymphoid tissue (MALT) lymphoma, a rarer non-Hodgkin lymphoma. While H. pylori infection is a significant factor, not every infected individual will develop cancer. Globally, about 70% of all gastric cancer cases are directly attributed to prior H. pylori infection, and the majority of gastric MALT lymphomas are also linked to this bacterium.
Understanding the Cancer Risk
Despite H. pylori being a known cause of stomach cancer, the absolute lifetime risk for most infected individuals remains relatively low, typically ranging from 1% to 3% for gastric adenocarcinoma. Several factors influence an individual’s risk. Certain H. pylori strains, particularly those carrying the CagA (cytotoxin-associated gene A) protein, are associated with an increased risk of gastric cancer.
Host genetic predispositions also play a role, with polymorphisms in immune-related genes, such as interleukin-1 beta (IL-1β), increasing susceptibility. Inherited mutations in certain genes can also elevate stomach cancer risk in infected individuals. Environmental factors, including diets high in salt and processed meats, as well as smoking, can further modify the risk. The progression from H. pylori infection to cancer is a multi-step, slow process, often involving decades of chronic inflammation and precancerous changes in the stomach lining.
How H. pylori Drives Cancer Development
H. pylori infection drives cancer development primarily through chronic inflammation within the stomach lining. This persistent inflammatory state leads to oxidative stress and the production of reactive oxygen species, which can damage the DNA of gastric cells. Over time, this cellular damage and ongoing inflammation disrupt normal cell growth, leading to DNA mutations and genomic instability. The bacterium’s virulence factors, such as the CagA protein, are injected into host cells, where they interfere with cellular signaling pathways and promote inflammation and uncontrolled cell proliferation.
The repeated cycles of inflammation, damage, and repair can cause the stomach lining to undergo a series of precancerous changes, often described as the “Correa cascade.” This cascade progresses through several stages before the development of gastric adenocarcinoma. For gastric MALT lymphoma, chronic inflammation triggers an abnormal accumulation and proliferation of immune B-cells in the stomach lining. This prolonged stimulation and genetic changes within these B-cells can eventually transform them into malignant lymphoma cells.
Managing H. pylori to Lower Cancer Risk
Diagnosis and treatment of H. pylori are important, particularly for individuals with symptoms or those at higher risk for stomach cancer. Common diagnostic methods include non-invasive tests like urea breath tests and stool antigen tests, which detect active infection. In some cases, an upper endoscopy with a biopsy of the stomach lining may be performed for direct detection and to assess for precancerous changes.
Standard treatment for H. pylori infection typically involves a combination of two or more antibiotics along with an acid-suppressing medication, such as a proton pump inhibitor, taken for one to two weeks. Successful eradication of the bacterium can significantly reduce the risk of developing stomach cancer. Clearing the infection can lower the risk of gastric cancer by approximately 50% to 75%, especially if treated early, before significant precancerous changes have occurred. While treatment reduces the risk, some increased risk may persist if precancerous changes were already present.