Scientist gets 1.4m pound to find how cancer steals keys from

Image
Press Trust of India London
Last Updated : Sep 18 2017 | 8:22 PM IST
A British scientist has received a 1.4 million pound fund to carry out pioneering research that could discover how cancer steals the keys from the body's locksmiths, disrupting healthy cell growth and function.
Dr Mathew Coleman, of the Institute of Cancer and Genomic Sciences at the University of Birmingham, will receive 1.4 million pound over six years from Cancer Research UK to find out more about three specific proteins that are thought to have a role in cancer.
The study by Coleman's group, which focuses on gastrointestinal cancer but the findings would likely be applicable to a variety of other tumour types, will be conducted on both human tissue and cells donated by cancer patients.
The proteins in our body come in all shapes and sizes and play a range of roles, including controlling energy production, cell growth and cell function, Coleman said.
But if these proteins become faulty, it can affect how they work, causing them and cells to go out of control.
"We are interested in three particular proteins, which are all enzymes that act as locksmiths for other proteins. Usually, these enzymes, called oxygenases, work by attaching an oxygen molecule to specific parts of other proteins, which generally turns them on," he said.
This is like a locksmith putting a key in a lock once the door is opened, it unlocks processes in a cell that ensure it develops normally and that everything is properly controlled, he added.
The scientist said that these enzyme locksmiths become faulty in cancer, which means they are unable to attach oxygen molecules to other proteins properly. This means the door remains shut, and certain processes are locked out.
"We think that this can lead to abnormal cell growth and function, which can lead to cancer. It's as if cancer has stolen the keys from these locksmiths.
"What is amazing is that such a small thing not being able to place a key in a lock has the potential to have a domino effect that disrupts cell growth and function, causing cells to go awry and turn cancerous," the scientist said.
Coleman's group will study both human tissue and cells donated by cancer patients who have generously given permission for their tumour samples to be used in research.
The hope is that by understanding how these oxygenases become faulty, and what goes wrong in cancer cells because they are not working properly, Coleman and his team may be able to find out how to regain control of wayward processes, leading to new targeted treatments for cancer patients.
Every week, around 600 people are diagnosed with cancer in the UK's West Midlands region.

Disclaimer: No Business Standard Journalist was involved in creation of this content

*Subscribe to Business Standard digital and get complimentary access to The New York Times

Smart Quarterly

₹900

3 Months

₹300/Month

SAVE 25%

Smart Essential

₹2,700

1 Year

₹225/Month

SAVE 46%
*Complimentary New York Times access for the 2nd year will be given after 12 months

Super Saver

₹3,900

2 Years

₹162/Month

Subscribe

Renews automatically, cancel anytime

Here’s what’s included in our digital subscription plans

Exclusive premium stories online

  • Over 30 premium stories daily, handpicked by our editors

Complimentary Access to The New York Times

  • News, Games, Cooking, Audio, Wirecutter & The Athletic

Business Standard Epaper

  • Digital replica of our daily newspaper — with options to read, save, and share

Curated Newsletters

  • Insights on markets, finance, politics, tech, and more delivered to your inbox

Market Analysis & Investment Insights

  • In-depth market analysis & insights with access to The Smart Investor

Archives

  • Repository of articles and publications dating back to 1997

Ad-free Reading

  • Uninterrupted reading experience with no advertisements

Seamless Access Across All Devices

  • Access Business Standard across devices — mobile, tablet, or PC, via web or app

More From This Section

First Published: Sep 18 2017 | 8:22 PM IST

Next Story