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Epigenetic Dysregulation at the Crossroad of Women’s Cancer

1
Cancer Biology Program, Rajiv Gandhi Centre for Biotechnology, Trivandrum, Kerala 695014, India
2
Department of Medicine, Division of Hematology-Oncology, Rutgers New Jersey Medical School, Newark, NJ 07103, USA
3
Department of Human and Molecular Genetics, Virginia Commonwealth University School of Medicine, Richmond, VA 23298, USA
4
Graduate Degree Program, Manipal Academy of Higher Education, Manipal, Karnataka 576104, India
*
Author to whom correspondence should be addressed.
Cancers 2019, 11(8), 1193; https://doi.org/10.3390/cancers11081193
Received: 2 June 2019 / Revised: 7 August 2019 / Accepted: 8 August 2019 / Published: 16 August 2019
An increasingly number of women of all age groups are affected by cancer, despite substantial progress in our understanding of cancer pathobiology, the underlying genomic alterations and signaling cascades, and cellular-environmental interactions. Though our understanding of women’s cancer is far more complete than ever before, there is no comprehensive model to explain the reasons behind the increased incidents of certain reproductive cancer among older as well as younger women. It is generally suspected that environmental and life-style factors affecting hormonal and growth control pathways might help account for the rise of women’s cancers in younger age, as well, via epigenetic mechanisms. Epigenetic regulators play an important role in orchestrating an orderly coordination of cellular signals in gene activity in response to upstream signaling and/or epigenetic modifiers present in a dynamic extracellular milieu. Here we will discuss the broad principles of epigenetic regulation of DNA methylation and demethylation, histone acetylation and deacetylation, and RNA methylation in women’s cancers in the context of gene expression, hormonal action, and the EGFR family of cell surface receptor tyrosine kinases. We anticipate that a better understanding of the epigenetics of women’s cancers may provide new regulatory leads and further fuel the development of new epigenetic biomarkers and therapeutic approaches. View Full-Text
Keywords: women cancer; methylation; acetylation; histones; RNA methylation; epitranscriptomics; chromatin; TET enzymes; receptor tyrosine kinases; estrogen receptor signaling women cancer; methylation; acetylation; histones; RNA methylation; epitranscriptomics; chromatin; TET enzymes; receptor tyrosine kinases; estrogen receptor signaling
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MDPI and ACS Style

Kumar, R.; Paul, A.M.; Rameshwar, P.; Pillai, M.R. Epigenetic Dysregulation at the Crossroad of Women’s Cancer. Cancers 2019, 11, 1193. https://doi.org/10.3390/cancers11081193

AMA Style

Kumar R, Paul AM, Rameshwar P, Pillai MR. Epigenetic Dysregulation at the Crossroad of Women’s Cancer. Cancers. 2019; 11(8):1193. https://doi.org/10.3390/cancers11081193

Chicago/Turabian Style

Kumar, Rakesh; Paul, Aswathy M.; Rameshwar, Pranela; Pillai, M. R. 2019. "Epigenetic Dysregulation at the Crossroad of Women’s Cancer" Cancers 11, no. 8: 1193. https://doi.org/10.3390/cancers11081193

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