Abstract
Hydroquinone (HQ), an active metabolite of benzene, plays an important role in the malignant hematopathy caused by benzene. Malignant transformation has been observed after 20 or 29 weeks of in vitro exposure to HQ and two years of in vivo exposure to HQ. Many epigenetic events have been identified in the process of HQ-induced mutations, suggesting that epigenetic changes may play important roles in the onset and process of HQ-induced carcinogenesis. In this review, we for the first time summarize the epigenetic mechanisms identified following exposure to HQ to provide more potential biomarkers and targets for the diagnosis and treatment of malignant hematopathy induced by benzene and its metabolites. The identified epigenetic changes are as follows: global DNA hypomethylation; hypomethylation of the thrombopoietin receptor MPL proto-oncogene; hypermethylation of the Rb and PTEN tumor suppressor genes; hypermethylation of erythroid-specific genes; enzymology of DNA methylation; phosphorylation, acetylation, and methylation of histones; aberrant expression of miRNAs and lncRNAs; and chromatin remodeling.
Graphical Abstract
Acknowledgements
The authors acknowledge the language assistance of Dr. Zhang.
Disclosure statement
No potential conflict of interest was reported by the author(s).