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Aziz et al. Cancer Drug Resist 2020;3:113-6 Cancer
DOI: 10.20517/cdr.2020.06 Drug Resistance

Editorial Open Access

Epigenetic basis of cancer drug resistance

Moammir H. Aziz , Aamir Ahmad 2
1
1 James H. Quillen VA Medical Center, Johnson City, TN 37604, USA.
2 School of Medicine, University of Alabama at Birmingham, Birmingham, AL 35205, USA.

Correspondence to: Dr. Aamir Ahmad, School of Medicine, University of Alabama at Birmingham, 901 19th St S, 370 BMRII,
Birmingham, AL 35205, USA. E-mail: aamirahmad@uabmc.edu

How to cite this article: Aziz MH, Ahmad A. Epigenetic basis of cancer drug resistance. Cancer Drug Resist 2020;3:113-6.
http://dx.doi.org/10.20517/cdr.2020.06
Received: 23 Jan 2020 Accepted: 31 Jan 2020 Published: 19 Mar 2020

Science Editor: Frits Peters Copy Editor: Jing-Wen Zhang Production Editor: Jing Yu

Cancer is a deadly disease and resistance to therapies is a major reason that renders it particularly
lethal. A majority of research thus far has focused on genetic factors that form the basis of cancer drug
resistance. However, it is increasingly being realized that epigenetic regulation plays a very important
role in determining the resistance of individual tumors to certain therapies. Several novel drugs that
target epigenetic events are under investigation, thus serving as a testimony to the enormous potential
of exploiting epigenetics in tackling the problem of cancer drug resistance. Moving forward, a focus on
epigenetics will be critical for a better understanding of the phenomenon of cancer drug resistance and for
the design of novel therapies.

Some cancer patients are inherently resistant to specific therapy because of their genetic makeup (de novo
cancer drug resistance) while other cancer patients initially respond to therapy, but eventually develop
[1]
resistance with continued administration (acquired cancer drug resistance) . A good understanding of
cancer drug resistance is critical to the efficient management of cancer patients in the clinics. Epigenetic
[2,3]
events have a profound effect on the onset as well as progression of human cancers . Methylation and
acetylation are two well-studied epigenetic events that are known to profoundly affect the expression
of genes, resulting in activation of oncogenes and/or suppression of tumor suppressor genes, leading to
development of cancer drug resistance. DNA methylation, histone modifications (methylation, acetylation,
phosphorylation, ubiquitylation, sumoylation, etc.), and regulation through microRNAs (miRNAs) are
some of the active areas of cancer research, encompassing the epigenetic regulation (see the Special Issue
on: Non-coding RNAs in Response and Resistance to Therapy in Cancer).

© The Author(s) 2020. Open Access This article is licensed under a Creative Commons Attribution 4.0
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