Articles related to PANCREATIC CANCER

This 1.25-credit CME course provides a review and update of current practice on minimally invasive vs. open pancreaticoduodenectomy, including trends and outcomes in robotic and laparoscopic pancreaticoduodenectomy.

The poor showing for immunotherapy in PDAC is likely a result of the cancer’s complex immunosuppressive tumor microenvironment, acting to insulate the tumor against an effective cytotoxic immune response. This review summarizes the mechanisms of immunosuppression within the PDAC tumor microenvironment and provides an up-to-date review of completed and ongoing clinical trials using various immunotherapy strategies.

The 18-month OS rates in this trial were: 66.7% for neoadjuvant mFOLFIRINOX 47.3% for neoadjuvant mFOLFIRINOX and hypofractionated radiotherapy 87.5% for mFOLFIRINOX followed by pancreatectomy 78.9% for mFOLFIRINOX plus radiotherapy followed by pancreatectomy The authors state these results “suggest that mFOLFIRINOX represents a reference neoadjuvant treatment regimen for borderline resectable pancreatic cancer; however, the role of radiotherapy in this setting remains undefined.”

This is a 1.75-hour credit expert round-table featuring members of UPMC faculty. The group dialogue together on the state-of the art in pancreatic cancer and their experience in biliary stenting including advantages of metal versus plastic stenting, and their experience in recent advances in molecular testing of pancreatic cysts, identifying those patients that will benefit from targeted surveillance of pancreatic cancer, and methods of performing PDAC surveillance and their outcomes. They also discuss prevention and management of post-op complications, and pain control in this population.

This Radiopedia entry updated in April provides a concise summary of clinical and radiographic features of pNETs and an outline of classification and treatment. In addition to the summary information, there are a score of CT and PET CT studies to explore.

When tested in mice with pancreatic cancer, a BET inhibitor/anti-PD-1 combination prevented neoplastic transformation induced by the oncogene KRAS, increased survival and increased the recruitment of cytotoxic T-cells to the tumor.