MAY 18, 2019 4:44 PM PDT

How a Cancer Drug Inhibits DNA Repair in Cancer Cells

WRITTEN BY: Nouran Amin

In a study published in the journal Science Translational Medicine, combing a certain cancer drug with other agents could potentially deliver a lethal blow in cancer that uses a specific pathway to create DNA repair cells.

Learn more about DNA repair and damage:

That drug is called Cediranib and when combined with another cancer agent known as olaparib (registered as Lynparza) can be effective in a specific form of ovarian cancer.

"The use of cediranib to help stop cancer cells from repairing damage to their DNA could potentially be useful in a number of cancers that rely on the pathway the drug targets," said the study's lead investigator, Alanna Kaplan. "If we could identify the cancers that depend on this pathway, we may be able to target a number of tumors."

Cediranib inhibits vascular endothelial growth factor (VEGF) receptors that stimulate the formation of blood vessels that support tumor growth. However, it has been less beneficial than the FDA-approved Avastin--an VEGF pathway inhibitor. On the other hand, Olaparib--the first approved DNA repair drug, inhibits a DNA repair enzyme called PARP which eradicates cancer cells with DNA defects in DNA repair from mutations in two DNA repair genes--BRCA1 and BRCA2.

DNA illustration. Credit: © Kirsty Pargeter / Adobe Stock

"There is a lot of interest in the cancer field in developing DNA repair inhibitors because they will greatly help treatments, like radiotherapy and chemotherapy, that aim to destroy DNA in cancer cells," said the senior author of the study, Peter M. Glazer, M.D. "People are recognizing that manipulating DNA repair could be very advantageous to boosting the benefit of traditional cancer treatment."

However, the combination of cediranib and olaparib was effective in ovarian cancers that did not include BRCA1/BRCA2 mutations. This lead to the launch of several clinical trials that tested the drug in duo for different types of cancers, such as prostate and lung cancer.

"The goal now is to investigate how we can broaden the potential of this synthetic lethality to other cancer types," said Glazer.

Source: Yale University News

 

About the Author
BS/MS
Nouran is a scientist, educator, and life-long learner with a passion for making science more communicable. When not busy in the lab isolating blood macrophages, she enjoys writing on various STEM topics.
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