Among the most resistant forms of breast cancer, triple-negative tumors carrying TP53 mutations have long confounded oncologists — but researchers at Baylor College of Medicine, working with partners in London and Brazil, have found that a genetic loss long associated with treatment failure may itself be the key to a new therapeutic opening. The absence of the LIG1 gene, which ordinarily helps cancer cells repair DNA damage, leaves those same cells dependent on alternative repair pathways — pathways that can now be blocked simultaneously with a two-drug combination. In this way, what appeared