Abstract
Pancreatic cancer (PC) is one of the most lethal forms of cancer, characterized by its aggressiveness and metastatic potential. Despite significant improvements in PC treatment and management, the complexity of the molecular pathways underlying its development has severely limited the available therapeutic opportunities. Toll-like receptors (TLRs) play a pivotal role in inflammation and immune response, as they are involved in pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs). Activation of TLRs initiates a signaling cascade, which in turn, leads to the transcription of several genes involved in inflammation and anti-microbial defense. TLRs are also deregulated in several cancers and can be used as prognostic markers and potential targets for cancer-targeted therapy. In this review we discuss the current knowledge about the role of TLRs in PC progression, focusing on the available TLRs-targeting compounds and their possible use in PC therapy.
Highlights
We report the current knowledge about the role of Toll-like receptors (TLRs) in Pancreatic cancer (PC) progression and we describe the compounds that may be implied in = PC treatment
The stimulation of TLR4 and CAP1 receptors with Resistin, a hormone released by macrophages in the cancer microenvironment, activates the STAT3 pathway that confers to pancreatic cancer cells the ability to resist cancer therapy [54]
Emerging evidence demonstrates that inflammation and pancreatic cancer are strongly associated
Summary
The standard treatment for patients affected by PC is surgical resection followed by chemotherapy This strategy, supported by different studies, results in the improvement of survival outcome. Dual treatment with capecitabine and gemcitabine after tumor resection results in the amelioration of the median overall survival [5] Another therapeutic approach that is often applied to PC patients is the administration of FOLFIRINOX (5FU, leucovorin, irinotecan and oxaliplatin). This latter strategy appears to lead to a higher overall survival, progression-free survival and response rate when compared to gemcitabine single treatment [6].
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