Immunomodulatory antitumor effect of interferon‑beta combined with gemcitabine in pancreatic cancer.

Resistance to gemcitabine is common and critically limits its therapeutic efficacy in patients with pancreatic cancer. Interferon‑beta (IFN‑β) induces numerous antitumor effects and synergizes with gemcitabine treatment. The immunomodulatory effects of this treatment regimen have not yet been described.

The Class I HDAC Inhibitor Valproic Acid Strongly Potentiates Gemcitabine Efficacy in Pancreatic Cancer by Immune System Activation.

Background: Gemcitabine efficacy in pancreatic cancer is often impaired due to limited intracellular uptake and metabolic activation. Epi-drugs target gene expression patterns and represent a promising approach to reverse chemoresistance. In this study, we investigate the chemosensitizing effect of different epi-drugs when combined with gemcitabine in pancreatic cancer.

Type I interferons in pancreatic cancer and development of new therapeutic approaches.

Immunotherapy has emerged as a new treatment strategy for cancer. However, its promise in pancreatic cancer has not yet been realized. Understanding the immunosuppressive tumor microenvironment of pancreatic cancer, and identifying new therapeutic targets to increase tumor-specific immune responses, is necessary in order to improve clinical outcomes.

Interferon-beta enhances sensitivity to gemcitabine in pancreatic cancer.

Background: Adjuvant gemcitabine for pancreatic cancer has limited efficacy in the clinical setting. Impaired drug metabolism is associated with treatment resistance. We aimed to evaluate the chemosensitising effect of interferon-beta (IFN-β).