CCMB finds gene responsible for pancreatitis

Researchers at the Centre for Cellular and Molecular Biology (CCMB) have been successful in identifying another marker gene, Cathepsin B (CTSB), that can be independently responsible for Tropical Calcific Pancreatitis (TCP), an acutely painful disease of the pancreas.

This is the second candidate gene after SPINK1, discovered in 2002, that is likely to independently cause this disease.

The new discovery has the potential for the development of a genetic screening test for susceptibility to chronic pancreatitis. This would help in early and accurate detection and modification of the course of the disease by early treatment and preventive measures such as change in food habits and lifestyle.

Addressing mediapersons, CCMB director Lalji Singh said, "There are a lot of people in our country, quite young in age, who are prone to TCP that leads to pancreatic cancer. The path-breaking new discovery could provide a predictive and preventive cure by early detection and thereby modifying the course of the disease." Efforts are also on to find a cure by using pancreatic stem cells that could be available in a couple of years, Singh said.

The findings of the new discovery have been recently published online in the prestigious international medical journal, GUT, and the publication will be accompanied by a commentary, a rare honour for the authors.

The research was done by a team led by Giriraj Ratan Chandak of CCMB in collaboration with a team of doctors led by D Nageshwar Reddy of the Asian Institute of Gastroenterology. The Indian Council for Medical Research (ICMR) and Council for Scientific and Industrial Research (CSIR) provided financial support.

In an earlier study published in 2002, besides establishing the genetic basis of TCP, it was found that mutation of the SPINK1 gene, an inhibitor of active trypsin inside the pancreas, was responsible for TCP. It has been found that persistence of active trypsin in the pancreas may result in the degeneration of pancreas, by the pancreas digesting itself. But the SPINK1 gene alone could not explain all the causes of TCP.

The present discovery found that a mutation in the CTSB gene prematurely activated trypsinogen and thereby maintained a constant supply of active trypsin in the pancreas, leading to TCP.