A*STAR scientists identify cause of chronic inflammation in human cancers

SINGAPORE : Scientists from the Agency for Science, Technology and Research (A*STAR) have identified the enzyme, telomerase, as a cause of chronic inflammation in human cancers.

A*STAR said this discovery holds the potential to reduce healthcare costs for many common inflammatory diseases such as cancer and diabetes.

Chronic inflammation is now recognised as a key underlying cause for the development of many human cancers, autoimmune disorders, neurodegenerative diseases and metabolic diseases such as diabetes.

This enzyme, which is known to be responsible for providing cancer cells the endless ability to divide, is now found to also jumpstart and maintain chronic inflammation in cancers.

In identifying this enzyme, inflammation can be prevented or reduced, and the common ailments can be alleviated.

A*STAR said this breakthrough is important as it shows how targeting telomerase with drugs could potentially reduce inflammation and hence get rid of cancer cells.

This discovery has a considerable impact on healthcare because developing drugs to target telomerase can greatly reduce healthcare costs.

Currently, the annual costs and expenses associated with cancer and metabolic diseases such as diabetes amount to about US$132 billion in the US alone.

Although many safe and effective anti—inflammatory drugs such as aspirin are currently available on the market, these drugs sometimes have side effects because blocking inflammation is typically detrimental to normal physiology.

So there is a need for the development of cost—effective drugs that are targeted, so as to minimise side effects.

This collaborative research was conducted by scientists at A*STAR’s Institute of Molecular and Cell Biology (IMCB) led by Assoc Prof Vinay Tergaonkar, A*STAR’s Genome Institute of Singapore (GIS) and National University of Singapore.

Other clinical collaborators include the Cancer Science Institute of Singapore and Duke—NUS Graduate Medical School.

The research findings were published on 18 November 2012 in the scientific journal Nature Cell Biology.

— CNA/ms