Bhubaneswar, April 28:
Indian scientists at Columbia University in the US have challenged a decade-old dogma in cancer biology by showing that a gene critical for preventing cancer did not work as thought of previously.
Healthy individuals have a normal variety of this gene, commonly known as A20. However, individuals develop cancer if the gene cannot function properly. Thus, many cancer patients are known to carry a dysfunctional variety of the gene.
So, the scientists created the first animal model of A20 to understand how this gene works in the body. Based on results over the past decade, they expected that these animals would develop cancer.
But to their surprise, they found that the animals had a largely healthy life-span.
The work was carried out by Indian scientist Arnab De, during his doctorate study at Columbia University with renowned Indian-American immunologist Sankar Ghosh.
The work was recently published as a highlighted article in European Molecular Biology Organization (EMBO) Reports, a peer-reviewed scientific journal that covers research related to biology at a molecular level.
Articles chosen to be highlighted by EMBO are considered to be of “fundamental relevance to a general readership”.
“I am hopeful that our work would contribute in a meaningful way towards testing cancer drugs in animals” De, who is now a senior scientist at AbbVie Bioresearch Center (formerly known as Abbott Laboratories), told IANS over phone on Tuesday.
Henning Walczak, scientific director of Cancer Research UK and chairman of Cancer Biology at University College London, reacting to this publication, said in an e-mail: “In healthy individuals, A20, also known as TNFAIP3, works beneficially to clear invading microbes. However, if A20 cannot function as a result of hereditary mutations or infection, it results in serious pathologies, including cancer.”
“Before this work, there was no animal model to understand how this critical tumour suppressor works. Having an animal model now, significantly improves our ability to investigate how A20 works, and this study already goes a long way in clarifying how A20 fails to work properly in patients and, as a consequence thereof, in developing potential cancer therapeutics”, he concludes.
Chozha Rathinam and Teruki Dainichi, currently at Kyoto University (Japan), are the other authors in this publication.
Cancers figure among the leading causes of morbidity and mortality worldwide, with approximately 14 million new cases and 8.2 million cancer related deaths in 2012, according to the World Health Organisation (WHO). The number of new cases is expected to rise by about 70 per cent over the next 2 decades, according to WHO. (IANS)