Penn Pancreatic Cancer Research Center

PCRC Team at PurpleStride November 4, 2017 (Kneeling in front row, PCRC Director Dr. Ben Z. Stanger and team captain Trish Gambino, RN)

Community Outreach in 2019

Patient Advocacy Day, Washington, D.C. June 25, 2019

Precision Promise Presentation with Pancreatic Cancer Action Network - June 5, 2019

Purple Light event April 28, 2019

Purple Stride Philadelphia 2019

Let's Win! Benefit in NYC

Beatty lab probes the molecular basis of liver metastasis

Pancreatic cancers frequently metastasize to the liver, and a new study from the Beatty laboratory shows that hepatocytes – the major cell type in the liver – plays a role in the process. Using a mouse model of pancreatic cancer, first author Jae Lee found that in animals with pancreatic tumors, hepatocytes had increased levels of the STAT3 molecule, which in turn caused them produce another protein, SAA, leading to enhanced metastasis. The study suggests that it may be possible to block this chain of events, reducing the overall burden of metastasis in the disease. Read more about it here.

Philadelphia Inquirer Feature

PCRC Researchers Drs. Kim Reiss-Binder and Mark O'Hara are featured in The Philadelphia Inquirer for leading studies that show exciting potential in combating Pancreatic Cancer. Read the article here.

Promising Clinical Data presented at AACR Meeting 2019

PCRC Researcher Mark O’Hara, M.D. presented exciting Phase 1 data regarding treatment of metastatic pancreatic cancer with combination immunotherapy (Gemcitabine, nab-paclitaxel, CD40 agonist, PD-1 antagonist). Watch the webcast here.

Wellen laboratory identifies new links between metabolic pathways and tumor growth

The Kras oncogene, which is mutated in the vast majority of pancreatic tumors, promotes cancer cell growth by activating a variety of signaling pathways. In this paper from Carrer and colleagues in Katy Wellen’s laboratory in the Abramson Cancer Center, the authors identify an increase in the abundance of an essential metabolite – acetyl-CoA – as a mechanism by which Kras promotes tumor formation. These studies provide a rationale for targeting the enzymes that supply tumor cells with abundant acetyl-CoA as a future approach to treating pancreatic cancer patients. Read more about it here.

 

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