The Role of Histone Deacetylase (HDAC) and EZH2 in Oncogenesis: Epigenetic Silencing of Tumor Suppressors

Junpei Yamaguchi, Motoko Sasaki, MD, PhD and Yasuni Nakanuma
Kanazawa University Graduate School of Medicine, Kanazawa, Japan, and others

Series: Cancer Etiology, Diagnosis and Treatments
BISAC: MED062000

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Volume 10

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Special issue: Resilience in breaking the cycle of children’s environmental health disparities
Edited by I Leslie Rubin, Robert J Geller, Abby Mutic, Benjamin A Gitterman, Nathan Mutic, Wayne Garfinkel, Claire D Coles, Kurt Martinuzzi, and Joav Merrick

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Epigenetic mechanisms result in the silencing of genes without a change in their coding sequence. The most well-characterized alteration is DNA hypermethylation, and a modification of histones also contributes to tumor suppressor loss through epigenetic silencing. Acetylation and deacetylation of histones play an important role in transcription regulation. The acetylation status of histones is determined by histone deacetylase (HDAC), and HDAC are strongly expressed in cancerous tissue. HDAC inhibitors are known to alter gene expression and to induce different phenotypes in various transformed cells, including growth arrest, apoptotic pathways and mitotic cell death. This book discusses the role of histone deacetylase and EZH2 in oncogenesis. (Imprint: Nova)

Abstract

Introduction

Epigenetic modifications

Cancer and epigenetics

HDACs and HDAC inhibitors

Polycomb group protein

Interaction of HDAC and EZH2

Epigenetic therapy

Conclusion

References

Index

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