Scientists found the single switch flipped by mutations behind a fifth of all cancers

Mutations in a protein complex called BAF turn up in about 20% of human cancers — lymphoma, breast, ovarian, liver and more — but nobody knew what single thing they all did. A Weill Cornell Medicine team, publishing in Nature, now has the answer: losing BAF flings open the folded architecture of DNA to a regulator protein called CTCF, which rewires gene activity toward faster cell division. In animal models, deleting CTCF reversed the effect — and in patient data, disrupted CTCF was linked to better outcomes. That makes CTCF and its partner complexes, PBAF and ISWI, candidate drug targets for a whole family of cancers at once. 'We hope before long to find a drug that blocks this process,' said co-lead author Dr Darko Barisic.

SDG 3 · Good health and well-being — Mechanism: tech innovation