In 1994 the International Agency for Research on Cancer (IARC) declared H. pylori a definite carcinogen. This was a big step. Very few “definite” carcinogens have been identified, even though trillions of research dollars have been spent and millions of scientists and physicians have devoted their entire careers to the study and treatment of this disease by determining the absolute best h. pylori diet. This label places H. pylori in a class with such infamous agents as cigarette smoke, asbestos, and UV and ionizing radiation. Unfortunately, however, the fact that the label has been applied does not mean that we truly understand how H. pylori works its mischief in the production of cancer. What it does mean, though, is that the association between infection and cancer is sufficiently strong (through clinical and epidemiological studies) and the scientific rationale so clear that a definite link can be made.

Before we can begin to understand the role that H. pylori may play in causing gastric and duodenal cancer and intestinal lymphoma, we must first discuss what cancer is and how it forms. Although we tend to discuss cancer as though it were a single disease, cancer is not really one disease; it is actually hundreds of diseases, all with different compositions and life histories. In fact, even for a given organ there are different types of cancer that may form, depending on the cells involved and the process that the tissue underwent during development of the disease. So, what is cancer? Cancer is a disease in which the cells of an organ or tissue lose their ability to recognize the normal signals that the body and neighboring cells send out to direct their growth, function, and death. Under normal circumstances, a balance of cell growth and cell death keeps the size of the cell population more or less constant. This cell death is a key physiological process known as apoptosis. An appropriate balance of cell growth and apoptosis is a crucial dynamic in the maintenance of healthy tissue, and cancerous tissues typically have alterations in one or both of these processes, that are, increased cell growth and/or decreased apoptosis.

The structure of the tissue is also crucial in keeping its cells functioning properly. Normal cells in healthy tissue maintain tight physical connections to their neighbors and respond to signals that they receive from the blood or adjacent cells. And, except for those in a few tissues (e.g., hair, intestine, blood), constituent cells do not divide rapidly; they divide only in response to the death or injury of a neighboring cell. This close physical and chemical communication instructs cells regarding what the tissue and organism require, and closely regulates their behavior.

All of this cellular anarchy leads to a loss of normal function in the tissue. Thus, the normal cells of the tissue, most of which do not divide rapidly, are pushed aside or are otherwise squeezed out and replaced by cells that function abnormally, divide too rapidly, and are resistant to apoptosis. The organ then loses its function and the person who carries the tumor begins to exhibit symptoms of its failure. Cancer is usually defined by its location (brain cancer, liver cancer, breast cancer, etc.), by the microscopic appearance of its cells, and by the degree to which it has spread (or metastasized). This geographic type of division makes sense; knowing in which organ the cancer has developed tells the physician a good deal about the disease’s life history and likely outcome. It also reveals something about how it could have arisen. For example, lung cancer in a smoker is not surprising, nor is melanoma in a sun-worshipper.

Agents that induce mutations in genes are called mutagens. These agents differ widely in their makeup and activity. They may be chemicals (like benzene), viruses (like human papilloma virus or hepatitis C), bacteria (like H. pylori), other agents like asbestos (a mineral fiber once used in insulation), or ionizing or UV radiation. Different classes of mutagens may act very differently in the precise manner by which they cause mutations. Some act directly on DNA, such as benzene, which damages DNA, or radiation, which breaks DNA; others, like H. pylori, act both directly and indirectly. The next step in the process of carcinogenesis is called promotion. This can be a non-mutational change that sets the cellular replication machinery in motion by triggering chemical reactions inside the cell that tell it to replicate its DNA and divide. By itself, excess replication does not lead to cancer; it is just one way by which most mutated cells expand their numbers. However, it is the genetic events that occur during and after that expansion of mutated cells that actually lead to the development of cancer.