Here is what a new study found.
Washington: Turns out, bacteria play an important role in driving sporadic colon cancer.
According to a study, patients with an inherited form of colon cancer harbour two bacterial species that collaborate to encourage the development of the disease, and the same species have been found in people who develop a sporadic form of colon cancer.
The study was led by a team of researchers from a Johns Hopkins Bloomberg-Kimmel Institute for Cancer Immunotherapy.
A second study on mice was published concurrently by the same researchers showed a possible mechanism behind how one of these species spurs a specific type of immune response, promoting--instead of inhibiting--the formation of malignant tumours.
Together, these findings could lead to new ways to more effectively screen for and ultimately prevent colon cancer, a disease that kills more than 50,000 people each year in the U.S. and is on the rise among younger adults age 20 to 50.
The Science findings described a process in which these bacteria invade the protective mucus layer of the colon and collude to create a microenvironment--complete with nutrients and everything the bacteria need to survive--that induces chronic inflammation and subsequent DNA damage that supports tumour formation.
These findings suggested a change in the standard of care for people who carry both types of bacteria.
"More frequent colon cancer screening than the currently recommended once every 10 years should be considered," said researcher Drew Pardoll.
Ultimately, once better understood, administering drugs or vaccines to prevent colonization of the bacteria in the colon, and potentially even probiotics to chase the bugs from the colon, are some of the preventive measures that could be explored to interrupt the cancer-promoting process.
These new findings by researcher Cynthia Sears are built upon her earlier research showing that particular strains of bacteria can invade the colon mucus in at least half of patients who get colon cancer but who have no inherited predisposition for the disease.
About 5 percent of colon cancers are caused by a hereditary syndrome called Familial Adenomatous Polyposis (FAP), in which an inherited mutation launches a series of genetic changes that develop over time and eventually prompt the epithelial cells to turn malignant.
However, Sears said, it was unclear whether ETBF or other bacteria played a role in the progression to colon cancer in FAP patients.
She said these same approaches could be applied to the more common sporadic types of colon cancer, which occur without a familial predisposition. Currently, colonoscopy to monitor for the formation of precancerous tumours, called polyps, is the standard of care.
Together, Sears said, the two new studies suggested a variety of strategies that researchers could test to prevent or even combat colon cancer. For example, it may be possible to prevent this disease by keeping the colon from becoming colonized by these two problematic bacteria, or by devising drugs or vaccines that target their toxins.
The study is published online on February 1st issue of Cell Host & Microbe and in the February 2nd issue of Science of John Hopkins Medicine.