Cancers emerge from many different paths. One path begins early, in embryonic development, when a protein complex called PRC2, which regulates cell differentiation, identity, and plasticity, becomes dysfunctional. PRC2 has well-established links to breast, prostate, blood, and skin cancers, among others.

It turns out that a small region of the complex long considered merely structural actually makes the entire protein function. And when researchers removed the region, called the SBD, the cancers they tested were stopped in their tracks.

“The SBD serves as a mechanical switch necessary for both healthy embryonic development and the maintenance of certain malignancies,” says lead author Agata Patriotis, a former member of the Allis lab and now a postdoc at the Koch Institute for Integrative Cancer Research at MIT. “This domain could potentially be targeted by cancer inhibitors.”