A study in this month's issue of the journal Gastroenterology, reveals that GCC, a protein receptor on the surface of intestinal epithelial cells for two hormones, guanylin and uroguanylin, can indeed subdue tumour formation. These hormones are the ones that regulate the growth of the intestinal cells.
In early stages of the disease, these growth-controlling hormones are deactivated. This disrupts GCC's activity and contributes to tumour formation, says lead author Scott Waldman of Jefferson Medical College.
In conclusion, the study findings "converts colon cancer from a genetic disease, which is the way we've all thought about it, to a disease of hormone insufficiency," says Waldman. "It's a completely different way of thinking about the disease", he points out.
Using two separate mouse models that mimic the development of colon cancer in people, researchers showed that GCC signaling blocks cancerous tumours from forming in the colon. When GCC was removed from the mice and a carcinogen introduced, researchers found tumours larger and in greater number in both the colon and intestines.
The same situation occurred in mice that carried a mutation of the APC gene, which causes the growth of colon polyps that lead to colon cancer.
Putting them together, exposure to a carcinogen or mutations in APC, along with the loss of GCC signaling is "a recipe for colon cancer," Waldman says.
Riding on the wave of this discovery, researchers would like to further show that by treating patients with hormone replacement therapy, intestinal cancer formation can either be prevented or treated.