| Literature DB >> 34606846 |
Dingzhi Wang1, Carlos S Cabalag2, Nicholas J Clemons3, Raymond N DuBois4.
Abstract
Chronic inflammation is a known risk factor for gastrointestinal cancer. The evidence that nonsteroidal anti-inflammatory drugs suppress the incidence, growth, and metastasis of gastrointestinal cancer supports the concept that a nonsteroidal anti-inflammatory drug target, cyclooxygenase, and its downstream bioactive lipid products may provide one of the links between inflammation and cancer. Preclinical studies have demonstrated that the cyclooxygenase-2-prostaglandin E2 pathway can promote gastrointestinal cancer development. Although the role of this pathway in cancer has been investigated extensively for 2 decades, only recent studies have described its effects on host defenses against transformed epithelial cells. Overcoming tumor-immune evasion remains one of the major challenges in cancer immunotherapy. This review summarizes the impacts of the cyclooxygenase-2-prostaglandin E2 pathway on gastrointestinal cancer development. Our focus was to highlight recent advances in our understanding of how this pathway induces tumor immune evasion. CrownEntities:
Keywords: Cancer-Associated Fibroblasts; Colorectal Cancer; Cyclooxygenase-2; Esophageal Cancer; Gastric Cancer; Prostaglandin E2; Tumor Immune Evasion; Tumor-Associated Angiogenesis
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Year: 2021 PMID: 34606846 DOI: 10.1053/j.gastro.2021.09.059
Source DB: PubMed Journal: Gastroenterology ISSN: 0016-5085 Impact factor: 22.682