Unifying mechanism explains how common cancer mutations fuel growth
A family of mutations seen in about 20% of human cancers drives malignancy by changing the accessibility of genes to a particular regulatory protein, according to a study by Weill Cornell Medicine investigators. The findings suggest new therapeutic strategies for a variety of cancer types.
A study published in Nature on October 28 reveals a unifying mechanism behind a common group of cancer mutations that drive malignancy. These mutations, found in approximately 20% of human cancers, alter the accessibility of genes to a protein called the BAF complex. The BAF complex, which regulates gene activity, is encoded by more than two dozen genes across the human genome.
Researchers from Weill Cornell Medicine, Memorial Sloan Kettering Cancer Center, and The Rockefeller University discovered that BAF mutations allow DNA's three-dimensional structure to be reshaped by the protein CTCF, leading to the activation of genes that promote cancer growth. Deleting CTCF in animal models reversed this effect, suggesting that CTCF and its partner proteins PBAF and ISWI could be targeted for new cancer therapies.
This finding establishes a common mechanism for a wide range of cancers, providing potential targets for future treatments.
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