Researchers have known that in up to one in 10 pancreatic cancer cases, a strange thing happens: some of the pancreatic cells appear to have lost their identity. “This is bizarre. You see pancreatic cancer, which usually somewhat resembles the original organ, losing those features and basically becoming akin to skin or esophagus—these other unrelated tissues,” explains Diogo Maia-Silva, PhD, a former postdoc at Cold Spring Harbor Lab (CSHL) and now at Massachusetts General Hospital.
Now, however, Maia-Silva and colleagues at CSHL just published a study “ ” in that details how the MED12 protein may play a critical role in this process. While the discovery is notable in and of itself, it also builds on decades of CSHL research. Twenty-five years ago, Alea Hills, PhD, discovered that —small cells in the lower part of the epidermis.
Later research from another CSHL professor. Christopher Vako, PhD, found that this protein can also cause . Exactly how was unclear.
Maia-Silva joined Vakoc’s lab in 2018, wanting to continue this investigation. Because p63 is notoriously difficult to target with drugs, he wondered which other molecules it might work with to confuse cells. With his colleagues, he developed a method to screen the entire genome of basal-like cancer cells and rank which genes were most important for maintaining their new identity.
In all his tests, rose to the top. This gene contains instructions for making the MED12 protein, one of about 25 in a complex th.
