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Cancer Epigenetics: An Introduction

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Cancer Epigenetics

Part of the book series: Methods in Molecular Biology ((MIMB,volume 1238))

Abstract

Epigenetic and genetic alterations contribute to cancer initiation and progression. Epigenetics refers to the study of heritable changes in gene expression without alterations in DNA sequences. Epigenetic changes are reversible and include key processes of DNA methylation, chromatin modifications, nucleosome positioning, and alterations in noncoding RNA profiles. Disruptions in epigenetic processes can lead to altered gene function and cellular neoplastic transformation. Epigenetic modifications precede genetic changes and usually occur at an early stage in neoplastic development. Recent technological advances offer a better understanding of the underlying epigenetic alterations during carcinogenesis and provide insight into the discovery of putative epigenetic biomarkers for detection, prognosis, risk assessment, and disease monitoring. In this chapter we provide information on various epigenetic mechanisms and their role in carcinogenesis, in particular, epigenetic modifications causing genetic changes and the potential clinical impact of epigenetic research in the future.

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Abbreviations

5adC:

5-Aza-2-deoxycytidine

8-OHdG:

8-Hydroxy-2′-deoxyguanosine

APC:

Adenomatosis polyposis coli

BRCA1:

Breast cancer1

CDH1:

Cadherin-1

ChIP:

Chromatin immunoprecipitation

DAPK1:

Death-associated protein kinase

DNA:

Deoxyribonucleic acid

DNMT:

DNA methyltransferase

DPP6:

Dipeptidyl-peptidase 6

EZH2:

Enhancer of zeste homolog 2

FHIT:

Fragile histidine triad protein

GADD45:

Growth arrest and DNA-damage-inducible protein GADD45 gamma

GSTP1:

Glutathione S-transferase pi 1

HATs:

Histone acetyltransferases

HDAC:

Histone deacetylase

HDMs:

Histone demethylases

HIC1:

Hypermethylated in cancer-1

HMTases:

Histone methyltransferases

HOX:

Homeobox

IGF:

Insulin-like growth factor

JARID1C:

Jumonji/ARID domain-containing protein 1C

JMDJ3:

Histone H3 lysine-27 demethylase

KLF4:

Kruppel-like factor 4

LINE:

Long interspread transposable element

LOI:

Loss of imprinting

MAGE :

Melanoma-associated gene

MBD:

Methyl-CpG-binding domain

MeCP:

Methyl-cytosine-binding protein

methyl H3K4:

Histone H3 lysine 4 methylation

methyl H3K9:

Histone H3 lysine 9 methylation

MGMT:

O6-methylguanine–DNA methyltransferase

miR:

microRNA

MLH1:

Mismatch repair gene 1

MYOD1:

Myogenic differentiation 1

OCT4:

Octamer-binding transcription factor 4

PTEN:

Phosphatase and tensin homolog

PTENP1:

Phosphatase and tensin homolog pseudogene 1

RAR:

Retinoic acid receptor

RARB2:

Retinoic acid receptor b2

RASSF1:

Ras association (RalGDS/AF-6) domain family member 1

Rb:

Retinoblastoma

RNA:

Ribonucleic acid

SETD2:

SET domain containing 2

SINE:

Short interspread transposable elements

SIRT1:

Silent information regulator type1

SOX2:

SRY (sex-determining region Y)-box 2

TMPRSS2:

Transmembrane protease serine 2

TMS1:

Target of methylation-induced silencing1

TRD:

Transcription repression domain

TSA:

Trichostatin A

UBE2C:

Ubiquitin-conjugating enzyme

UTX:

Ubiquitously transcribed tetratricopeptide repeat X chromosome

WRN:

Werner syndrome RecQ helikase like

WWOX:

WW domain-containing oxidoreductase

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Acknowledgements

The reference from author’s laboratory listed in this review was supported by United States Public Health Service Grants RO1 CA115491, RO1 CA108512, and R21 CA109424. We apologize to those investigators whose original work could not be cited owing to the space limitations.

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Correspondence to Sanjay Gupta Ph.D. .

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Kanwal, R., Gupta, K., Gupta, S. (2015). Cancer Epigenetics: An Introduction. In: Verma, M. (eds) Cancer Epigenetics. Methods in Molecular Biology, vol 1238. Humana Press, New York, NY. https://doi.org/10.1007/978-1-4939-1804-1_1

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  • DOI: https://doi.org/10.1007/978-1-4939-1804-1_1

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