Antibiotic Novobiocin found to kill tumor cells with DNA-repair glitch - Dana-Farber Cancer Institute | Boston, MA
Please note that some translations using Google Translate may not be accurately represented and downloaded documents cannot be translated. Dana-Farber assumes no liability for inaccuracies that may result from using this third-party tool, which is for website translation and not clinical interactions. You may request a live medical interpreter for a discussion about your care.
An antibiotic developed in the 1950s and largely supplanted by newer drugs, effectively targets and kills cancer cells with a common genetic defect, laboratory research by Dana-Farber Cancer Institute scientists shows. The findings have spurred investigators to open a clinical trial of the drug, novobiocin, for patients whose tumors carry the abnormality.
In a study in the journal Nature Cancer, the researchers found that in laboratory cell lines and tumor models novobiocin selectively killed tumor cells with abnormal BRCA1 or BRCA2 genes, which help repair damaged DNA. The drug was effective even in tumors resistant to agents known as PARP inhibitors, which have become a prime therapy for cancers with DNA-repair glitches.
“PARP inhibitors represent an important advance in the treatment of cancers with defects in BRCA1, BRCA2, or other genes involved in DNA repair. By allowing tumor cells to accumulate additional genetic damage, they essentially incapacitate the cells and cause them to die,” says Alan D’Andrea, MD, director of the Susan F. Smith Center for Women's Cancers and the Center for DNA Damage and Repair at Dana-Farber and co-senior author of the study with Raphael Ceccaldi, PhD, PharmD, of the Curie Institute in Paris. “They are effective for many patients, but the cancer eventually becomes resistant and begins growing again. Drugs capable of overcoming that resistance are urgently needed.” D’Andrea added.
