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Nutrigenomics: Epigenetics and cancer prevention: A comprehensive review

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Pages 1375-1387 | Published online: 07 Feb 2019
 

Abstract

Due to change in lifestyle and food habits, people are more at risk of diet-related diseases and cancers. It is also established that dietary modifications significantly reduce the risk of diseases. Nutrigenomics is relatively fresh discipline, but possess an enormous potential that can apply for prevention and management of certain carcinomas and diseases. This review enables us to generate useful information for scientists and health professionals regarding the role of Nutrigenomics in the prevention of diet and lifestyle-related diseases like cancer. It influences health conditions of individuals and susceptibility of disease by defining the metabolic response and gene expression. Epigenetic modifications can perform a significant role in disease occurrence and pathogenesis. DNA methylation and chromatin remodeling are the most common epigenetic mechanisms. Omega 3 fatty acids are the best example of nutrients and gene interaction not involving DNA methylation while certain bioactive food compounds have a proven role in cancer prevention through an epigenetic mechanism. Dietary polyphenols substantially take part in prevention of oral, breast, skin, esophageal, colorectal, prostate, pancreatic and lung cancers. Moreover, minerals and vitamins involve regulatory processes. Zinc, Selenium and folate involve in DNA repairing process have anticancer properties. Consumption of multivitamins prevents methylation of cancer cells.

Acknowledgments

The authors are thankful to all who facilitated us to complete this review and acknowledge the support of AIOU faculty from the department of home and health sciences Islamabad.

Financial and competing interests

There is no financial and competing interest of the authors in this publication.

Author contributions

Principle author Ayesha Nasir (RD) was involved in basic execution, design and write up of the article. Dr. Mir M Hassan Bullo (MBBS, MSPH) has given major input in the write-up, advance execution and formatting of the article. Esha yaqoob was engaged in the literature search. While the final review was completed by the Dr. Zaheer Ahmed (MPhil Ph.D.), Dr. Mahpara Safdar (MPhil, Ph.D.) and Dr. Hajra Ahamed (MPhil, Ph.D.) at AIOU Islamabad.

Abbreviations

AA=

Arachidonic acid

AIOU=

Allama Iqbal Open University

BRCA1=

Breast Cancer Susceptibility Gene 1

BTG3=

B-cell Translocation Gene 3

COMT=

Catechol-O-Methyltransferase

COX-2=

Cyclooxygenase 2

CpG=

Cytosine-phosphate- Guanine

DHA=

Docosahexaenoic Acid

DNA=

Deoxyribonucleic Acid

DNMT=

Deoxyribonucleic Acid Methyltransferase

EGCG=

Epigallocatechin Gallate

EPA=

Eicosapentaenoic Acid

GSTP1=

Glutathione S-Transferase Pi 1

(GWAS)=

Genome-wide association studies

H3=

Histone 3

H4=

Histone 4

HAT=

Histone Acetyltransferase

HDAC=

Histone Deacetylase

HAT=

Histone Acetyltransferase

H3K9=

Histone 3 Lysine 9

hMLH1=

Human MutL Homolog 1

hTERT=

Human Telomerase Reverse Transcriptase

MBD2=

Methyl Binding Domain

MCF-7=

Michigan Cancer Foundation 7 cells

MGMT=

O-6-Methylguanine-DNA-Methyltransferas

mRNA=

Messenger Ribonucleic Acid

NTCD=

Neural Tube Closure Defects

NSALDs=

Non-Steroidal Anti Inflammatory Drugs

RARB=

Retinoic Acid Receptor Bet: ^$

D=

Registered Dietician

RNA=

Ribonucleic Acid

SAM=

S-Adenosyl Methionine

SAH=

S-Adenosyl-L-Homocysteine

TP 35=

Tumor Protein 35

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