Immune checkpoint and inflammation as therapeutic targets in pancreatic carcinoma

Abstract

Pancreatic adenocarcinoma (PAC) is one of the most deadly malignant neoplasms, and the efficacy of conventional cytotoxic chemotherapy is far from satisfactory. Recent research studies have revealed that immunosuppression and inflammation are associated with oncogenesis, as well as tumor development, invasion, and metastasis in PAC. Thus, immunosuppression-related signaling, especially that involving immune checkpoint and inflammation, has emerged as novel treatment targets for PAC. However, PAC is an immune-resistant tumor, and it is still unclear whether immune checkpoint or anti-inflammation therapies would be an ideal strategy. In this article, we will review immune checkpoint and inflammation as potential targets, as well as clinical trials and the prospects for immunotherapy in PAC.

Keywords: Immune checkpoint; Inflammation; Pancreatic adenocarcinoma; Randomized clinical trial; Therapeutic anticancer target.

Figure 1

Various inflammation-associated signaling pathways activated in Kras mutant pancreatic cancer cells, as novel treatment targets. CXCL5: C-X-C motif chemokine ligand 5; ERK: Extracellular signal-regulated kinase; IL: Interleukin; JAK: Janus kinase; NF-κB: Nuclear factor kappa-light-chain-enhancer of activated B cells; STAT: Signal transducer and activator of transcription; TNF: Tumor necrosis factor; TNF-R: TNF-receptor.