A new study has proved that gastrin levels have a very important role to play in the development of Helicobacter-induced stomach cancer.
Over 50 percent of the world's population is infected with Helicobacter pylori, which causes chronic inflammation of the stomach lining, and is strongly linked to the development of gastric ulcers and stomach cancer.
Stomach cancer is the second leading cause of cancer-related deaths worldwide.
Helicobacter infection results in increased expression of gastrin, a hormone that stimulates secretion of gastric acid.
However, the role of gastrin in cancer development still remains unclear.
While high levels of gastrin lead to the development of stomach cancer, but absence of gastrin has been shown to increase the numbers of tumours in the gastric antrum- the lower section of the stomach that empties into the small intestine.
Thus, for explaining this apparent disparity, a group led by Dr. Timothy Wang at the Columbia University Medical Center in New York, NY examined the contribution of Helicobacter infection to gastric cancer in animal models with either high expression of gastrin or no gastrin at all.
It was found that Helicobacter infection in mice with high levels of gastrin resulted in cancer of the gastric corpus (main body of the stomach).
On the other hand, infection in gastrin-deficient mice led to cancer in a different part of the stomach- the gastric antrum.
Thus, the researchers concluded that gastrin plays a key role in the development of Helicobacter-induced stomach cancer, but may have distinct effects on carcinogenesis in different parts of the stomach.
The related report by Takaishi et al, 'Gastrin is an essential cofactor for Helicobacter-associated gastric corpus carcinogenesis in C57BL/6 mice', is appearing in the upcoming issue of The American Journal of Pathology.