Colorectal cancer is the cause of death for some 600,000 people per year in the world and patient numbers are still increasing. Risk of colorectal cancer is greatly increased by inherited factors, lifestyle (smoking or alcohol consumption) and microbial infections causing bowel inflammation (colitis), the prolongation of which leads to tumorigenesis.
The mechanism by which chronic colitis develops into colorectal cancer was thought to involve the production of a range of bioactive substances by immune cells invading intestinal tissue in response to inflammation, which metabolic products then stimulate cells in inflamed tissue into abnormal (cancerous) growth. In other words, there would be a good chance of suppressing the emergence of colorectal cancer by treating the disease that causes the inflammation or preventing the inflammation from becoming chronic.
Associate Professor Takahisa Murata and his colleagues from the University of Tokyo’s Graduate School of Agricultural and Life Sciences have discovered an anti-inflammatory mediator in colitis and colon cancer. They found in mice that mast cells, a type of immune cell often observed inflamed colon tissue, produces the anti-inflammatory mediator prostaglandin D2 (PGD2) which reduces severity of inflammation and strongly inhibits tumor development. They also showed that treatment with a PGD2 receptor agonist that simulates release of PGD2 improves colitis and suppresses the emergence of colon cancer.
Their observations may lead to the development of new preventions and treatments for colon cancer and enteritis.
Source: University of Tokyo