New gene for ovarian cancer identified

Article

A faulty copy of the gene RAD51D significantly increases the likelihood of developing ovarian cancer, according to a study published online August 7 in Nature Genetics. MORE

A faulty copy of the gene RAD51D significantly increases the likelihood of developing ovarian cancer, according to a study published online August 7 in Nature Genetics.

When researchers from Britain’s Institute for Cancer Research compared the DNA of unrelated women from 911 families with ovarian and breast cancer with DNA from a control group of more than 1,060 people in the general population, they found that women with cancer had 8 faults in the RAD51D gene compared with only 1 in the control group.

The researchers also investigated the sensitivity of RAD51D-deficient cells to PARP inhibitors, a new class of drugs that interfere with the enzyme poly (adenosine-biphosphate [ADP]-ribose) polymerase. Developed to treat cancers caused by faults in the breast and ovarian cancer genes BRCA1 and BRCA2, the drugs work by blocking DNA repair mechanisms in cancer cells.

The study results “show that cells deficient in RAD51D are sensitive to treatment with a PARP inhibitor,” the authors write. “These data suggest that PARP inhibitors may have clinical utility in individuals with RAD51D mutations.”

To read the other articles in this issue of Special Delivery,click here.

Related Videos
Exploring the intersection of heart health and women's health | Image Credit: cedars-sinai.org
Unlocking the benefits of DHEA | Image Credit: drannacabeca.com
Unlocking the power of oxytocin | Image credit: drannacabeca.com
Revolutionizing menopause management: A deep dive into fezolinetant | Image Credit: uvahealth.com.
Deciding the best treatment for uterine fibroids | Image Credit: jeffersonhealth.org.
Clinical pearls of pediatric dermatology | Image Credit: profiles.ucsf.edu
Approaching inflammatory vulvovaginal diseases | Image Credit: profiles.ucsf.edu.
Related Content
© 2024 MJH Life Sciences

All rights reserved.