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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.

The study, published Oct. 28 in Nature, focused on a protein complex called the BAF complex, which regulates gene activity in the nucleus. Mutations in genes that encode subunits of this complex are found in tumors as different as lymphoma, breast cancer, ovarian cancer and liver cancer, but the common mechanism underlying this broad connection to cancers has been elusive.

In the study, the scientists showed that these BAF mutations effectively allow the three-dimensional architecture of DNA to be reshaped extensively by a protein called CTCF. This shifts gene activity in a direction that promotes malignancy, but deleting CTCF in an animal model reverses the effect.

"These findings help us establish a unifying mechanism for one of the most common classes of cancer mutations and identify CTCF and its partner proteins as candidate therapeutic targets in these cancers," said study co-corresponding author Dr. Darko Barisic, an assistant professor of cancer biology in medicine and a member of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine.

The other co-corresponding authors were Dr. Cem Meydan, assistant professor of research in systems and computational biomedicine at Weill Cornell Medicine, and Dr.

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