Make PEEC, not war: does evasive transdifferentiation protect from carcinogenesis?
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Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)
Published on: December 19, 2019
1Department of Dermatology, Venerology, and Allergology, University Medical Center Mannheim, Ruprecht-Karls University Heidelberg, Mannheim, Germany. sergij.goerdt@haut.ma.uni-heidelberg.de
Abstract:
DNA repair and immune surveillance are established mechanisms that secure a programmed escape from the evolution of cancer (PEEC) by healing and elimination, respectively. Evasive transdifferentiation, i.e. silencing of carcinogenic events, is an emerging concept with potentially broad applicability that paradigmatically includes the claim that common acquired melanocytic nevi represent a programmed rescue from malignity for initiated melanocytes. This hypothesis is difficult to test. Research into the molecular mechanisms that govern the development of acquired melanocytic nevi, however, should result in the identification of a molecular master switch and an associated set of genes that - beyond the processes involved in apoptosis - may help bypass carcinogenesis and may be of therapeutic benefit in the future.
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