Colorectal cancer is an epithelial cancer. The epithelial surface of the colon is organised into pits called crypts and projections called villi. The cells on the surface of the colon are damaged frequently due to friction with food passing through, and need to be replaced. Stem cells that constantly divide are located at the base of the crypts. This is because a signalling molecule called Wnt is situated here. When cells detect Wnt, then keep dividing. As they are pushed out of the crypt by other cells they can no longer detect any Wnt, and stop dividing. One of the first steps in colorectal cancer is that cells develop mutations that stop them responding to Wnt properly. They keep dividing and push all the normal cells out. Because they continue to divide the epithelium develops many more folds than it otherwise would. Because the cells divide more frequently they accumulate more mutations and start to reactivate genes that encourage proliferation. Aspirin can work via the Cox2 pathway to turn off some of these genes and potentially slow down the process. If colorectal cancer is not caught early and the polyps removed, it can spiral out of control into metastatic cancer.
This piece was created for Creative Reactions in collaboration with Professor Ann Williams from the University of Bristol.