A team of University of California, San Diego School of Medicine researchers has discovered that common intestinal bacteria appear to promote tumor growths in genetically susceptible mice, but that tumorigenesis can be suppressed if the mice are exposed to an inhibiting protein enzyme.
The research, said lead author Eyal Raz, MD, a professor of medicine at UC San Diego, could portend an eventual new form of treatment for people with familial adenomatous polyposis or FAP, an inherited condition in which numerous initially benign polyps form in the large intestine, eventually transforming into malignant colon cancer.
The research appears online May 9 in the journal Nature Medicine.
Raz, with colleagues at the UC San Diego School of Medicine and Wonkwang University in the Republic of Korea, looked at interactions between the vast numbers of bacteria typically found in the gastrointestinal tract and the tract's mucosal lining. Ordinarily, the bacteria and tract establish a kind of homeostasis. "In a normal host, these bacteria actually serve important roles, such as supporting cell production," said Raz. "But in susceptible hosts, the presence of these bacteria turns out to be detrimental."
Specifically, Raz and his co-authors found that mice with an engineered mutation that closely mimics FAP in humans leaves the mice notably vulnerable to inflammatory factors produced by ordinary bacterial activity. The constant inflammation enhances expression of an oncogene called c-Myc. Very quickly, the mice develop numerous tumors in their intestines and typically do not survive past six months of age.
In humans, FAP can be equally devastating. It is a genetic condition in which patients at a young age begin to develop hundreds to thousands of polyps in their intestine. By age 35, 95 percent of individuals with FAP have polyps. The polyps start out benign, but ultimately become malignant without treatment. Current treatmen
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University of California - San Diego