Heat-induced inflammation and its role in esophageal cancer.

Abstract

Esophageal cancer, the sixth most common cause of death from cancer worldwide, consists of different histological types and displays various patterns of incidence. Esophageal adenocarcinoma and esophageal squamous cell carcinoma are the most prevalent types. As epidemiological studies report that ingesting hot substances is one major risk factor for squamous cell carcinoma, evaluating the effect of this external stress on esophagus cells seems desirable. This specific kind of stress brings about cellular changes and stabilizes them by affecting different cellular features such as genetic stability, membrane integrity and the regulation of signaling pathways. It also causes tissue injury by affecting the extracellular matrix and cell viability. Thus, one of the main consequences of thermal injury is the activation of the immune system, which can result in chronic inflammation. The genetic alteration that has occurred during thermal injury and the consequent reduction in the function of repair systems is further strengthened by chronic inflammation, thereby increasing the probability that mutated cell lines may appear. The molecules that present in this circumstance, such as heat shock proteins, cytokines, chemokines and other inflammatory factors, affect intercellular signaling pathways, including nuclear factor kappa-light-chain-enhancer of activated B cells, signal transducer activator of transcription-3 and hypoxia-inducible factor 1α in supporting the survival and emergence of mutant phenotypes and the consequent malignant progression in altered cell lines. This investigation of these effective factors and their probable role in the tumorigenic path may improve current understanding.