黑料吃瓜资源

Cold Spring Harbor, NY — Cancer cells are often described as cells 鈥済one bad鈥� or 鈥渞enegade.鈥� New research reveals that in some of the deadliest cases of pancreatic cancer, these rebellious cells have an unexpected addiction. Now, scientists are investigating if that addiction can be used to bring about a tumor鈥檚 end.

黑料吃瓜资源 (CSHL) research recently published in the journal Cell Reports, investigated this addictive behavior of cancer cells in the most aggressive of pancreatic cancer subtypes.

鈥淭his version of the cancer is especially deadly,鈥� said lead author Timothy Somerville, a postdoctoral fellow in the lab of CSHL Professor Chris Vakoc, M.D., Ph.D.

He explained that the average pancreatic cancer patient will survive for about two years after diagnosis. However, a notable subgroup succumbs to the disease much earlier鈥攂efore the end of its first year. The Vakoc team suspects that a unique protein in the pancreas of these unfortunate patients is a cause.

鈥淲e were able to identify a gene [and the protein it produces] called Tumor-Protein 63 (TP63) that is specifically expressed in this aggressive form of pancreatic cancer,鈥� said Somerville.

Protein 63 (P63) is not normally present within pancreas cells. It is necessary for the creation of specialized cells called squamous cells. These are long, thin cells that are required for the formation of skin. When the researchers noticed P63 at work within the pancreas鈥攏owhere near the skin鈥攖hey knew something was suspicious. P63 was encouraging pancreas cells to grow into things they had no business being!

Further testing revealed that having this squamous-cell-promoting gene inappropriately active within the tumor was making it very easy for new renegade cells to arise and spread to other parts of the body. However, when something is easy, there鈥檚 usually a catch—even for cancer.

鈥淥ne of the encouraging findings is that when this happens… the cancer cells become so reliant on P63 that they actually require P63 for their continued growth,鈥� Somerville explained. 鈥淪o moving forward, we鈥檙e looking into approaches to suppress inappropriate P63 activity as a treatment option for patients.鈥�

Another goal of the Vakoc team is to discover why the TP63 gene gets active in the pancreas of specific patients in the first place. 鈥淚f we can stop it from ever happening,鈥� said Somerville, 鈥渋t could be really good for the survival of this most vulnerable group of cancer patients.鈥�

Written by: Brian Stallard, Content Developer/Communicator | [email protected] | 516-367-8455

Funding

This study was funded by the State of New York (contract number C150158), Pershing Square Sohn Cancer Research Alliance, Boehringer Ingelheim, Northwell Health Affiliation, NCI, the Pancreatic Cancer Action Network, the Lustgarten Foundation for Pancreatic Cancer Research, and NIH.

Citation

T. Somerville et. al., 鈥淭P63-mediated enhancer reprogramming drives the squamous subtype of pancreatic ductal adenocarcinoma鈥� was published in Cell Reports on November 13, 2018.