A major study by the research group of Dr. Josef Penninger, at the University of Toronto, has identified a protein that, when absent, appears to contribute to the development of colorectal cancer. The protein in question is the p110g catalytic subunit of phosphoinositide-3-OH kinases (PI(3)Ks), a family of proteins that regulate a vast array of fundamental cell responses, including proliferation, transformation, differentiation and protection from apoptosis. Quite by accident, the researchers discovered that genetic inactivation of the p110g subunit leads to the development of invasive colorectal carcinomas in mice. In humans it has been previously found that p110g protein expression is lost in primary colorectal adenocarcinomas and in colon cancer cell lines. Overexpressing wildtype or kinase-dead p110g in human colon cancer cell lines with mutations of tumour suppressors, or with the oncogenes b-catenin and Ki-ras, suppressed tumorigenesis.
Penninger's group was examining genetically altered mice to determine how their white blood cells responded to infection when the mice lost weight, became sick and began to die. It turned out that they were riddled with colon cancer. Turning this discovery into practical medicine for the treatment of colon cancer in humans will obviously require time and a lot more study. However, it is hoped that this knowledge may help in the design of novel strategies for fighting colon cancer.
Colon cancers are the second leading cause of cancer death and it is estimated that 50% of humans develop colon tumours by the age of 70.
Source
- Sasaki T, et al. Colorectal Carcinomas in Mice Lacking the Catalytic Subunit of PI(3)Kg Nature 2000 (406) 897-902.
