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Implication of the Strand-Specific Imprinting and Segregation Model: Integrating <em>in utero</em> Hormone Exposure, Stem Cell and Lateral Asymmetry Hypotheses in Breast Cancer Aetiology | Abstract
ISSN: 2161-1041

Hereditary Genetics: Current Research
Open Access

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Review Article

Implication of the Strand-Specific Imprinting and Segregation Model: Integrating in utero Hormone Exposure, Stem Cell and Lateral Asymmetry Hypotheses in Breast Cancer Aetiology

Singh Harbinder1, Carol A Lazzara1 and Amar JS Klar2*

1Department of Biological Sciences, Delaware State University, Dover, USA

2Gene Regulation and Chromosome Biology Laboratory, Frederick National Laboratory for Cancer Research, National Institutes of Health, Frederick, USA

*Corresponding Author:
Amar JS Klar
Section Head, Gene Regulation and Chromosome Biology laboratory
National Cancer Institute at Frederick, 7th Street
Ft. Detrick, P.O. Box B, Frederick, MD 21702, USA
Tel: 301 846 5916
Fax: 301 846 6911
E-mail: [email protected]

Received Date: May 31, 2013; Accepted Date: August 12, 2013; Published Date: August 16, 2013

Citation: Harbinder S, Lazzara CA, Klar AJS (2013) Implication of the Strand- Specific Imprinting and Segregation Model: Integrating in utero Hormone Exposure, Stem Cell and Lateral Asymmetry Hypotheses in Breast Cancer Aetiology. Genetics S2:005. doi: 10.4172/2161-1041.S2-005

Copyright: © 2013 Harbinder S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Known genetic mutations and familial hereditary factors account for less than 20–25% of breast cancer cases in women, therefore, most instances have been classified as sporadic cases of unknown aetiologies. Single nucleotide polymorphisms (SNPs) were considered as breast cancer risk factors, but numerous studies have failed to support this assertion. Recent evidence correlates aberrant epigenetic mechanisms in the development and metastatic progression of breast cancer, yet there has been limited progress made to identify the primary aetiology underlying sporadic cases of breast cancer. This has led some researchers to consider alternative hypotheses including in utero exposure to deleterious chemical agents during early development, the immortal strand and the strand-specific imprinting and selective chromatid segregation hypotheses. Here, we integrate prominent alternate models to help guide future research on this very important topic concerning human health.

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