Topic: Epigenetic Basis of Cancer Drug Resistance

A special issue of Cancer Drug Resistance.

ISSN 2578-532X (Online)

Submission deadline: 28 Feb 2019

Guest Editor(s)

  • Aamir Ahmad, PhD
    Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama, USA

    Website | E-mail

Special Issue Introduction

Cancer is a deadly disease and resistance to therapies is a major reason that renders it particularly lethal. 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 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. A majority of research so 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 in determining the resistance of individual tumors to certain therapies. 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) as well as regulation through microRNAs (miRNAs) are some of the active areas of cancer research, encompassing the epigenetic regulation. A number of 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.
This special issue welcomes novel research and detailed review articles addressing the progress made in our understanding of epigenetic basis of cancer drug resistance. This issue will also serve as a platform to discuss the promises as well as unique challenges specific to this field of cancer research. All the submitted articles will undergo rigorous peer review and will be published free of charge upon acceptance.


Cancer Drug Resistance; Epigenetic; Methylation; Demethylation; Acetylation; Deacetylation; Phosphorylation; Ubiquitylation; Sumoylation; microRNAs; Gene Silencing; Cancer Relapse

Submission Deadline

28 Feb 2019

Submission Information

Articles of special issue are free of charge for article processing.
For Author Instructions, please refer to
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Submission Deadline: 28 Feb 2019
Contacts: Elaine Gao, Managing Editor,


The following list shows the information of planned papers to this special issue. All the papers submitted to Cancer Drug Resistance will go through a rigorous peer review. (Please note that the information below is provisional and may be subject to future change)

Planned Papers

Type: Review

Title: The Role of Histone Lysine Demethylases in cancer cells' resistance to tyrosine kinase inhibitors

Authors: Perla Pucci, Francesco Crea, Jasmine Cassar White

Affiliations: Open University, Department of Life, Health and Chemical Sciences, Milton Keynes, United Kingdom

Abstract: Current cancer therapies are often associated with treatment failure and reduced patients’ survival due to drug resistance. There are various mechanisms involved in the acquisition of cancer drug resistance, including the selection of advantageous mutations, overexpression of transporter proteins and epigenetic alterations. In this context, epigenetic alterations refer to chromatin-mediated regulation of gene expression that results in heritable changes in the cellular phenotype. There is an ever-growing body of evidence suggesting that epigenetic mechanisms play an important role in bringing about drug resistance in cancer cells. While the relationship between chemotherapy and epigenetics has been widely discussed, emerging evidence indicates that specific epigenetic effectors are also crucial for the development of resistance to tyrosine kinase inhibitors (TKIs). One particular gene that encodes the histone lysine demethylase KDM5A is overexpressed in several cancers. In breast cancer tissues, cells with KDM5A gene amplification were found to be more resistant to erlotinib, an inhibitor of the tyrosine kinase epidermal growth factor receptor (EGFR), when compared to cells without the same amplification. KDM5A was also shown to mediate resistance to a second EGFR inhibitor called gefitinib, in EGFR-mutant lung cancer cell lines. This evidence indicates that KDM5A could activate alternative survival pathways involved in overcoming EGFR inhibition. In line with these results, another histone demethylase (i.e. KDM1A) promotes liver cancer cells’ resistance to the TKI sorafenib. Current evidence provides a suitable rationale to consider the use of specific KDMs inhibitors to sensitize cells to tyrosine kinase targeted therapies and thus, presents an opportunity to prevent the further development of drug resistance. This review discusses the involvement of histone lysine demethylases in the development of resistance to TKI and highlights the importance to develop new cancer treatment regimens to combat this phenomenon.

Type: Review

Title: Epigenetic changes, centrosome and cancer drug resistance

Authors: Epigenetic changes, centrosome and cancer drug resistance Authors: Zanhui Jia1, Xinggang Wang2 and Hong Zhang2,3

1. Second Hospital of Jilin University, Changchun, China.
2. Department of Biomedicine (DBM), University Hospital, University of Basel, Switzerland.
3. To whom correspondence should be sent

Abstract: The centrosome is an organelle that plays an importent role in the regulation of cell cycle progression, ensuring the normality of cell division. It composed of two centrioles surrounded by hundreds of proteins making up of the pericentriolar material (PMC). Epigenetic modifications can lead to centrosome aberrations, such as disorganized spindles and centrosome amplification causing aneuploidy and genomic instability. Therefore centrosome defects found in pre-neoplasias and many cancers. Epigenetic disturbances are associated not only with carcinogenesis and cancer progression, but also with resistance to chemotherapy. Clinical trials involving new drugs against centrosome proteins have shown promising results, suggesting that targeting centrosome aberrations may be beneficial in sensitizing cancer cells to other drugs.

Published Articles