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PREFACE

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 therapies because of their genetic makeup (de novo cancer drug resistance)
while other cancer patients initially respond to therapies, 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 role 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.), and regulation through microRNAs (miRNAs) are some
of the active areas of cancer research, encompassing the epigenetic regulation. A number of novel drugs, which 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 book on the epigenetic basis of cancer drug resistance touches upon some very diverse and hot topics
that detail the current progress in understanding the importance of epigenetic events in determining the resistance against
various therapies and in a number of different cancers. Without such understanding, the design of novel therapies to counter
drug resistance would be impossible.

Aamir Ahmad
Special Issue Editor