New Findings from Henry Ford Cancer Institute Describe Advances in Xenografts (BUB1 regulates non-homologous end joining pathway to mediate radioresistance in triple-negative breast cancer).

New research from the Henry Ford Cancer Institute explores the role of BUB1, a cell cycle kinase, in radioresistance in triple-negative breast cancer (TNBC). TNBC is a highly aggressive form of breast cancer that is often treated with radiotherapy. The study found that BUB1 is overexpressed in TNBC and its inhibition sensitizes TNBC cells to radiation, leading to increased cell killing. BUB1 ablation also resulted in radiosensitization in TNBC tumor xenografts. The findings suggest that BUB1 could be a novel molecular target for radiosensitization in women with TNBC. [Extracted from the article]

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