Dear Voornaam,

Welcome to the Cancer Grand Challenges newsletter, your update on news, research and opportunities to get involved. Weve included you in this newsletter because we think our new challenges might interest you if you'd rather not receive this in the future, just let us know.

Today marks the launch of an ambitious new round of challenges each with the potential to make radical progress against cancer. Were delighted to share these with you below, read on for more information.

Four global, multidisciplinary teams will each receive 20M to solve one of these challenges. If you have what it takes, build your dream team and embark on a mission with the power to create real change. Find more details here and apply by 22 April 2021.

This month were also delighted to welcome to the scientific committee Professor Jill Mesirov and Professor Barbara Rimer, bringing with them a wealth of academic excellence. Meet Jill and Barbara here.

Finally, you might have noticed the new look and feel of this newsletter, reflecting our new partnership with the National Cancer Institute and our bold global ambition for Cancer Grand Challenges. Check out our new website and follow us on Twitter and LinkedIn to keep up to date with the latest news.

Best wishes,
The Cancer Grand Challenges team

MUTOGRAPHS: NEW PERSPECTIVES ON HOW CANCER DEVELOPS

For years, research has focussed on mutations damage to our DNA as the driving cause of cancer. But were starting to appreciate that mutations are not the only piece of the puzzle: recent studies have shown cells can carry hundreds or even thousands of mutations and still appear normal.

In a new study, researchers from the Mutographs team investigated 20 known or suspected carcinogens and their effect on mouse DNA. All induced cancer but, strikingly, only 3 of 20 caused distinct DNA damage. The remaining 17 drove tumour growth without causing damage to DNA, instead promoting key cellular processes or altering a cells environment.

A major step forward in putting the pieces of the puzzle together, the findings could dramatically improve our understanding of what causes cancer to develop, transforming our ability to prevent and treat the disease.

OPTIMISTICC: NEW CONNECTION DRIVES POOR OUTCOMES IN BOWEL CANCER

Up to 45% of bowel cancers carry a fault in the KRAS gene, detrimentally affecting how a patient will respond to treatment. New results from the OPTIMISTICC team suggest these poor outcomes may be due to the way faulty KRAS interacts with another molecule, the IL-22 receptor.

IL-22 normally plays a vital role in keeping the bowel healthy, ensuring its cells grow and divide at a normal rate. But the findings suggest this combination of features high levels of the IL-22 receptor and a faulty KRAS can cause uncontrollable division of bowel cells, driving tumour development.

Unfortunately, people whose bowel cancer carries both features are predicted to respond less well to current treatments and are more likely to relapse. But testing for both features could identify high-risk patients, ensuring they are monitored closely. And blocking the IL-22 receptor could provide a new, unexplored treatment option for these people.