Inhibition of Interleukin-10 in the tumor microenvironment can restore mesothelin chimeric antigen receptor T cell activity in pancreatic cancer in vitro.

Background: Pancreatic cancer cells are known to shield themselves from immunosurveillance by secreting immune inhibitory cytokines such as Interleukin-10. Using mesothelin, a differentiating antigen that is overexpressed in pancreatic cancer, we assessed the negative effect of the tumor microenvironment on chimeric antigen receptor T cell-based immunotherapy and its reversal via depletion of Interleukin-10.

Methods: T cells cultured in pancreatic cancer-cell-conditioned medium were transduced with lentiviruses encoding mesothelin-chimeric antigen receptor in the presence or absence of anti-Interleukin-10-blocking antibody.

Enhanced phosphorylation of p53 by microRNA-26a leading to growth inhibition of pancreatic cancer.

Purpose: MicroRNA (miR)-26a has been identified as a tumor suppressor in pancreatic cancer cells. Although wild-type p53 controls cell-cycle progression, its mutant form normally present in pancreatic cancer loses this capability. Phosphorylation is known to restore wild-type activity to mutant p53.

Radiofrequency ablation offers a reliable surgical modality for the treatment of Barrett's esophagus with a minimal learning curve.

Radiofrequency ablation (RFA) has gained popularity as treatment for Barrett's esophagus. Inclusive series of patients from initiation of our Barrett's Therapy Program were studied. Review of patients undergoing RFA for Barrett's was performed from September 2008 to May 2011.