New principle emerges for breast cancer chemotherapy resistance
Patients with breast cancer may have mutant BRCA1 or BRCA2 genes. These mutant proteins damage DNA surveyors, sensors and responders in normal cells. They also help the body repair damaged NDA through complex operations.
People with these mutant genes typically have defective DNA repair. This gives them greater chances of developing ovarian, breast and other cancers; between 20 and 25 percent of hereditary breast cancers are because of these mutants, in addition to 5-10 percent of all breast cancers.
Reducing the body’s repairs to damaged DNA may make these cells more sensitive to drugs that damage DNA. Scientists connected the DNA replication forks as a way that drug resistance grows in the mutant ovarian and breast cancers.
“It is the intricate mechanisms that tumor cells evolve to bypass the need for accurate DNA repair that form the foundation of our study,” Dr. Andre Nussenzweig, from the National Cancer Institute, said. “A deeper knowledge of the processes that drive drug resistance in BRCA1/2-mutant tumors will lead to novel therapeutic approaches that target tumor-specific vulnerabilities.”
The results of the study, which lasted 10 years, are available in the Nature journal.
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