A new study reveals that the MYC protein does more than drive tumor growth. It also repairs DNA damage in cancer cells, allowing some tumors to survive chemotherapy and radiation.
Researchers at Oregon Health & Science University found that MYC moves to sites of broken DNA and recruits repair proteins. This nontraditional role helps tumor cells recover from treatments meant to destroy them, according to senior author Rosalie Sears.
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Researchers at Penn State College of Medicine report that unusually high activity of the DNA-repair gene EXO1 can damage newly replicated DNA and create BRCA-like weaknesses in some tumors, potentially helping identify patients who could respond to certain treatments used for BRCA-mutant cancers.
Researchers at McGill University report a drug-based method to temporarily enhance natural killer (NK) cells—an immune cell type—by inhibiting two proteins, improving the cells’ ability to attack several aggressive cancers in preclinical experiments.
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A protein called NFIL3 has been identified as a key factor in reducing the long-term performance of CAR T cells used in cancer treatment. Researchers showed that disabling this protein allows the engineered cells to remain active longer and fight tumors more effectively in laboratory models.