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Environmentally-Mediated Epigenetic Effects: Uncovering the Fertile Soil in the Development of Pediatric Cancer

Received: 20 December 2016    Accepted: 30 December 2016    Published: 17 January 2017
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Abstract

Environmentally-induced epigenetic changes of gene regulation could result from chronic, lifelong exposure, to low doses of environmental toxicants, such as chemicals including, tobacco smoking and endocrine disrupting compounds, or to other environmental factors such as nutritional changes, and lifestyle-related conditions. These environmentally-acquired epigenetic marks may influence the control of gene regulation through DNA methylation, histone modification, or through a large set of non-coding RNAs (ncRNAs). These epigenetic effects might be passed on to the developing embryo and child as inheritable non-genetic marks, which recapitulate previous lifelong history of exposure to environmental influences that start from the stage of primordial germ cell, passing through the maturing germ cell, and ending by the zygote stage. This involves the paternally transmitted information on the sperm that contribute to modulating embryogenesis functions and later childhood development, in concert with, the maternally transmitted information encountered by the exposure to a large milieu of environmental factors either periconceptionally or during lactation period.

Published in International Journal of Clinical Oncology and Cancer Research (Volume 1, Issue 1)
DOI 10.11648/j.ijcocr.20160101.16
Page(s) 36-41
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Pediatric Oncology, Childhood Cancer, Epigenetics, Environmental Exposures, Epigenetic Inheritance & Evolution, Pediatric Cancer Susceptibility

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Cite This Article
  • APA Style

    Ahmed Mohammed Morsy, Eman Ahmed Hasan, Ameer Mohammed Abuelgheet, Ahmed Salaheldeen Hassan. (2017). Environmentally-Mediated Epigenetic Effects: Uncovering the Fertile Soil in the Development of Pediatric Cancer. International Journal of Clinical Oncology and Cancer Research, 1(1), 36-41. https://doi.org/10.11648/j.ijcocr.20160101.16

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    ACS Style

    Ahmed Mohammed Morsy; Eman Ahmed Hasan; Ameer Mohammed Abuelgheet; Ahmed Salaheldeen Hassan. Environmentally-Mediated Epigenetic Effects: Uncovering the Fertile Soil in the Development of Pediatric Cancer. Int. J. Clin. Oncol. Cancer Res. 2017, 1(1), 36-41. doi: 10.11648/j.ijcocr.20160101.16

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    AMA Style

    Ahmed Mohammed Morsy, Eman Ahmed Hasan, Ameer Mohammed Abuelgheet, Ahmed Salaheldeen Hassan. Environmentally-Mediated Epigenetic Effects: Uncovering the Fertile Soil in the Development of Pediatric Cancer. Int J Clin Oncol Cancer Res. 2017;1(1):36-41. doi: 10.11648/j.ijcocr.20160101.16

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  • @article{10.11648/j.ijcocr.20160101.16,
      author = {Ahmed Mohammed Morsy and Eman Ahmed Hasan and Ameer Mohammed Abuelgheet and Ahmed Salaheldeen Hassan},
      title = {Environmentally-Mediated Epigenetic Effects: Uncovering the Fertile Soil in the Development of Pediatric Cancer},
      journal = {International Journal of Clinical Oncology and Cancer Research},
      volume = {1},
      number = {1},
      pages = {36-41},
      doi = {10.11648/j.ijcocr.20160101.16},
      url = {https://doi.org/10.11648/j.ijcocr.20160101.16},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijcocr.20160101.16},
      abstract = {Environmentally-induced epigenetic changes of gene regulation could result from chronic, lifelong exposure, to low doses of environmental toxicants, such as chemicals including, tobacco smoking and endocrine disrupting compounds, or to other environmental factors such as nutritional changes, and lifestyle-related conditions. These environmentally-acquired epigenetic marks may influence the control of gene regulation through DNA methylation, histone modification, or through a large set of non-coding RNAs (ncRNAs). These epigenetic effects might be passed on to the developing embryo and child as inheritable non-genetic marks, which recapitulate previous lifelong history of exposure to environmental influences that start from the stage of primordial germ cell, passing through the maturing germ cell, and ending by the zygote stage. This involves the paternally transmitted information on the sperm that contribute to modulating embryogenesis functions and later childhood development, in concert with, the maternally transmitted information encountered by the exposure to a large milieu of environmental factors either periconceptionally or during lactation period.},
     year = {2017}
    }
    

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    AB  - Environmentally-induced epigenetic changes of gene regulation could result from chronic, lifelong exposure, to low doses of environmental toxicants, such as chemicals including, tobacco smoking and endocrine disrupting compounds, or to other environmental factors such as nutritional changes, and lifestyle-related conditions. These environmentally-acquired epigenetic marks may influence the control of gene regulation through DNA methylation, histone modification, or through a large set of non-coding RNAs (ncRNAs). These epigenetic effects might be passed on to the developing embryo and child as inheritable non-genetic marks, which recapitulate previous lifelong history of exposure to environmental influences that start from the stage of primordial germ cell, passing through the maturing germ cell, and ending by the zygote stage. This involves the paternally transmitted information on the sperm that contribute to modulating embryogenesis functions and later childhood development, in concert with, the maternally transmitted information encountered by the exposure to a large milieu of environmental factors either periconceptionally or during lactation period.
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Author Information
  • Pediatric Oncology Department, South Egypt Cancer Institute, Assiut University, Assiut, Egypt

  • Clinical Pathology Department, South Egypt Cancer Institute, Assiut University, Assiut, Egypt

  • Department of Pediatrics, Faculty of Medicine, Assiut University, Assiut, Egypt

  • Pediatric Oncology Department, South Egypt Cancer Institute, Assiut University, Assiut, Egypt

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