Indem Forscher die „Bodyguard“ -Rolle eines Protein -Duos bei Mäusen ausklopfen, haben sie eine versteckte Schwäche bei Bauchspeicheldrüsenkrebs ausgesetzt | Es ist eine Entdeckung, die zu schlauer und wirksameren Behandlungen für einen der tödlichsten Krebsarten führen könnte.

From the article: Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic cancer. With an overall survival rate of around 13%, it’s also one of the deadliest cancers. One reason for this is that the cancer is intrinsically resistant to nearly all forms of treatment, including chemotherapy, radiotherapy, and immunotherapy.

Now, though, a new [study](https://www.sciencedirect.com/science/article/pii/S2213231725003611?via%3Dihub) led by researchers from Indiana University’s (IU) School of Medicine has identified a way to weaken PDAC’s built-in defenses, offering a more effective treatment strategy for it and, potentially, other aggressive cancers.

“This research shows us a brand new vulnerability in pancreatic cancer,” said Melissa Fishel, PhD, study co-author and tumor cell biologist at the IU School of Medicine. “That opens the door to developing combination therapies that could work better than anything currently available, not just for pancreatic cancer but potentially for other aggressive cancers too.”

The researchers focused on two proteins they already knew were implicated in PDAC: redox effector factor-1 (Ref-1) and peroxiredoxin-1 (PRDX1). Both are abnormally abundant in pancreatic tumors compared with normal tissue and they work hand-in-hand to create resistance to treatment in pancreatic cancer cells. By studying Ref-1 and PRDX1 together, the researchers wanted to see if they could exploit this partnership, turning it into a therapeutic weakness.

Think of Ref-1 like a switchboard operator for cancer genes. Many cancer-driving transcription factors, which are proteins that bind to specific DNA sequences to control gene activity, need to be in the right chemical (redox) state to work. Ref-1 keeps them switched on, so they can turn up the activity of genes that help cancer cells grow, resist stress, and avoid dying. PRDX1 is, essentially, Ref-1’s bodyguard. Its main job is to clean up harmful molecules called reactive oxygen species (ROS), which build up in cells. By controlling the cell’s redox balance, PRDX1 makes sure Ref-1 can keep doing its job of activating cancer-driving genes. This “protection service” makes cancer cells tougher, because Ref-1 and its partners can keep the tumor alive even under stress.