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Yale University researchers have discovered that colonization by the common stomach bacteria Helicobacter pylori in people with non-O blood types is associated with a nearly 3-fold increased risk of pancreatic cancer.
The research, published online in the Journal of the National Cancer Institute, confirms the role of H pylori in the onset of pancreatic cancer. In the United States, pancreatic cancer is the fourth most frequent cause of cancer death, affecting more than 1% of the population. Known risk factors for pancreatic cancer include certain uncommon inherited genetic mutations, chronic pancreatitis, non-O (A, B, and AB) blood type, and cigarette smoking. Yet only 30% of the cases of pancreatic cancer can be attributed to these factors. Seven years ago, a research team from the Yale Cancer Center Prevention and Control Research Program proposed that colonization by H pylori increased the risk of pancreatic cancer by boosting stomach acidity as well as the pancreatic response to neutralize the acidity. Over the intervening years, the researchers carried out a large population-based, case-control study of pancreatic cancer in Connecticut and found that stomach colonization by strains of H pylori that cause increased gastric acidity is indeed associated with increased risk of pancreatic cancer. “Our results provide confirmation of the involvement of H pylori in the causation of pancreatic cancer, as well as suggest the pathway, from bacterial colonization, to excess stomach acidity, to increased pancreatic response, to enhanced susceptibility to smoking and other carcinogens, and finally to cancer transformation,” explained lead author and principal investigator Harvey Risch, MD, PhD, professor of epidemiology and public health at Yale. Drs. Herbert Yu, Lingeng Lu, and Mark Kidd are among the authors of this study, which was funded by the National Cancer Institute. The findings provide the first systematic explanation of how pancreatic cancer originates in the body. In addition, the research provides an estimation of the risk of developing the disease and lays the foundation for an in-depth exploration of the pathway of the disease.
(Source: Yale University Medical News, March 5, 2010.)
