We've updated our Privacy Policy to make it clearer how we use your personal data.

We use cookies to provide you with a better experience. You can read our Cookie Policy here.

Advertisement
Yale Team finds why BRCA Gene Resists Cancer Treatment
News

Yale Team finds why BRCA Gene Resists Cancer Treatment

Yale Team finds why BRCA Gene Resists Cancer Treatment
News

Yale Team finds why BRCA Gene Resists Cancer Treatment

Read time:
 

Want a FREE PDF version of This News Story?

Complete the form below and we will email you a PDF version of "Yale Team finds why BRCA Gene Resists Cancer Treatment"

First Name*
Last Name*
Email Address*
Country*
Company Type*
Job Function*
Would you like to receive further email communication from Technology Networks?

Technology Networks Ltd. needs the contact information you provide to us to contact you about our products and services. You may unsubscribe from these communications at any time. For information on how to unsubscribe, as well as our privacy practices and commitment to protecting your privacy, check out our Privacy Policy

Some mutant forms can lead to ovarian and breast cancer in as many as 6 in 10 women.

The findings suggest how biochemists might be able to decrease drug resistance to existing therapies that target this form of cancer, the authors report in the July 2 issue of the journal Molecular Cell.

“We can design specific targets for drug development only if we fully understand the key players and how they work in the pathway for repairing DNA breaks,” said Patrick Sung, professor in the Department of Molecular Biophysics and Biochemistry, researcher at the Yale Cancer Center, and senior author of the paper.

BRCA genes normally act to repair damaged DNA and suppress tumor formation. Variants of BRCA genes, however, are hijacked by cancer and have been recognized for decades as markers for increased risk of breast cancer, but they also play a role in ovarian, prostate, and pancreatic cancer.

Drugs that target DNA repair pathways in patients with BRCA mutations have proved effective in attacking cancer, but these patients tend to develop resistance to the drug. The cancer returns because the BRCA proteins develop secondary mutations, which continue to promote cancer growth.

The new paper establishes the crucial role played by co-factor DSS1, which mimics DNA that aids in the repair damage of cells. Without DSS1, BRCA2 variant cannot fulfill its normal duty of DNA repair crucial to survival of cancer. Drugs that interfere with DSS1 function could be developed and used in conjunction with existing drugs like Astra Zeneca’s Lynparza to overcome this resistance, Sung said.

Advertisement