Breast Cancer Cells Hijack DNA Process to Fight Effects of Chemotherapy, Study Finds

Breast Cancer Cells Hijack DNA Process to Fight Effects of Chemotherapy, Study Finds
Breast cancer cells with mutations in the BRCA1 or BRCA2 genes can become resistant to chemotherapy drugs by recruiting a host of proteins that protect tumor DNA from damage. Since mutations in the BRCA1 and BRCA2 genes cause flaws in DNA repair processes, increasing the risk of breast, ovarian, and other types of cancer, the study “Replication fork stability confers chemoresistance in BRCA-deficient cells,” published in the journal Nature, demonstrates how a tumor balances the need for new mutations with the ability to protect itself from extensive DNA damage. In the short term, the findings might allow physicians to predict the response to DNA-damaging chemotherapy by measuring the levels of these proteins. In a longer perspective, they may also help cancer scientists find ways around tumor resistance to chemotherapy, a serious problem in cancer treatment. The BRCA1 and BRCA2 genes code for proteins that continuously survey DNA, looking for and repairing damage. Mutations in these genes disrupt the process and are found in up to 10 percent of all breast cancer patients. While the mutations are the culprit causing cancer in the first place, the inability of BRCA1 and 2 to mend broken DNA also makes tumor cells particularly sensitive to DNA-damaging cancer treatment. Over time, however, many tumors become resistant to such drugs. Andre Nussenzweig, PhD, and his research team at the National Cancer Institute have been studying DNA repair processes for the past decade, and are focusing on the protection of DNA during replication, or DNA-copying. The process occurs at specific spots along the DNA strand cal
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