| Peer-Reviewed

Molecular Mechanisms Associated with Virus-induced Oncogenesis and Oncolysis

Received: 4 June 2019     Accepted: 13 July 2019     Published: 15 August 2019
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Abstract

Cancer is a leading cause of human deaths worldwide. Besides inherited genetic disorders, a diverse range of physical, chemical and biological agents may induce cancer. About 15-20% of cancers are known to be originated due to pathogens. Viruses are considered to be the second (after smoking) most important risk factor in inducing human cancer. Viruses may either harbour a copy of oncogene or have an ability to alter the expression of cellular copy of the oncogenes. Both RNA and DNA viruses are can induce oncogenesis. Most of the DNA tumour viruses either integrate their genome (complete or part of it) into the host genome or express early genes that are required for early event of virus replication. These early genes are responsible for oncogenic transformation of host cells. Based upon the mechanism involved, oncogenic RNA viruses are divided into two groups-transforming and non-transforming RNA viruses. Transforming RNA viruses carry viral oncogenes that are homologous to the host oncogene, their expression in infected cells results in oncogenic transformation of the cell. Non-transforming RNA viruses induce oncogenesis similar to the DNA viruses. Contrary, oncolytic viruses selectively replicate in cancerous cells and induce cell death without any damage to the normal tissues. Typically, oncolytic viruses are nonpathogenic to humans that can naturally replicate in cancer cells by exploiting oncogenic cell signalling pathways. Pathogenic viruses can also be genetically manipulated which allow them to replicate in cancerous but not in normal cells. This review review describes the molecular mechanisms associated with virus induced oncogenesis and oncolysis.

Published in Cancer Research Journal (Volume 7, Issue 3)
DOI 10.11648/j.crj.20190703.13
Page(s) 87-100
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), 2019. Published by Science Publishing Group

Keywords

Oncogenic, Oncolytic, Virus

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Cite This Article
  • APA Style

    Ram Kumar, Riyesh Thachamvally, Sunil Maherchandani, Bhupendra Nath Tripathi, Sanjay Barua, et al. (2019). Molecular Mechanisms Associated with Virus-induced Oncogenesis and Oncolysis. Cancer Research Journal, 7(3), 87-100. https://doi.org/10.11648/j.crj.20190703.13

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    ACS Style

    Ram Kumar; Riyesh Thachamvally; Sunil Maherchandani; Bhupendra Nath Tripathi; Sanjay Barua, et al. Molecular Mechanisms Associated with Virus-induced Oncogenesis and Oncolysis. Cancer Res. J. 2019, 7(3), 87-100. doi: 10.11648/j.crj.20190703.13

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    AMA Style

    Ram Kumar, Riyesh Thachamvally, Sunil Maherchandani, Bhupendra Nath Tripathi, Sanjay Barua, et al. Molecular Mechanisms Associated with Virus-induced Oncogenesis and Oncolysis. Cancer Res J. 2019;7(3):87-100. doi: 10.11648/j.crj.20190703.13

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  • @article{10.11648/j.crj.20190703.13,
      author = {Ram Kumar and Riyesh Thachamvally and Sunil Maherchandani and Bhupendra Nath Tripathi and Sanjay Barua and Naveen Kumar},
      title = {Molecular Mechanisms Associated with Virus-induced Oncogenesis and Oncolysis},
      journal = {Cancer Research Journal},
      volume = {7},
      number = {3},
      pages = {87-100},
      doi = {10.11648/j.crj.20190703.13},
      url = {https://doi.org/10.11648/j.crj.20190703.13},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.crj.20190703.13},
      abstract = {Cancer is a leading cause of human deaths worldwide. Besides inherited genetic disorders, a diverse range of physical, chemical and biological agents may induce cancer. About 15-20% of cancers are known to be originated due to pathogens. Viruses are considered to be the second (after smoking) most important risk factor in inducing human cancer. Viruses may either harbour a copy of oncogene or have an ability to alter the expression of cellular copy of the oncogenes. Both RNA and DNA viruses are can induce oncogenesis. Most of the DNA tumour viruses either integrate their genome (complete or part of it) into the host genome or express early genes that are required for early event of virus replication. These early genes are responsible for oncogenic transformation of host cells. Based upon the mechanism involved, oncogenic RNA viruses are divided into two groups-transforming and non-transforming RNA viruses. Transforming RNA viruses carry viral oncogenes that are homologous to the host oncogene, their expression in infected cells results in oncogenic transformation of the cell. Non-transforming RNA viruses induce oncogenesis similar to the DNA viruses. Contrary, oncolytic viruses selectively replicate in cancerous cells and induce cell death without any damage to the normal tissues. Typically, oncolytic viruses are nonpathogenic to humans that can naturally replicate in cancer cells by exploiting oncogenic cell signalling pathways. Pathogenic viruses can also be genetically manipulated which allow them to replicate in cancerous but not in normal cells. This review review describes the molecular mechanisms associated with virus induced oncogenesis and oncolysis.},
     year = {2019}
    }
    

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  • TY  - JOUR
    T1  - Molecular Mechanisms Associated with Virus-induced Oncogenesis and Oncolysis
    AU  - Ram Kumar
    AU  - Riyesh Thachamvally
    AU  - Sunil Maherchandani
    AU  - Bhupendra Nath Tripathi
    AU  - Sanjay Barua
    AU  - Naveen Kumar
    Y1  - 2019/08/15
    PY  - 2019
    N1  - https://doi.org/10.11648/j.crj.20190703.13
    DO  - 10.11648/j.crj.20190703.13
    T2  - Cancer Research Journal
    JF  - Cancer Research Journal
    JO  - Cancer Research Journal
    SP  - 87
    EP  - 100
    PB  - Science Publishing Group
    SN  - 2330-8214
    UR  - https://doi.org/10.11648/j.crj.20190703.13
    AB  - Cancer is a leading cause of human deaths worldwide. Besides inherited genetic disorders, a diverse range of physical, chemical and biological agents may induce cancer. About 15-20% of cancers are known to be originated due to pathogens. Viruses are considered to be the second (after smoking) most important risk factor in inducing human cancer. Viruses may either harbour a copy of oncogene or have an ability to alter the expression of cellular copy of the oncogenes. Both RNA and DNA viruses are can induce oncogenesis. Most of the DNA tumour viruses either integrate their genome (complete or part of it) into the host genome or express early genes that are required for early event of virus replication. These early genes are responsible for oncogenic transformation of host cells. Based upon the mechanism involved, oncogenic RNA viruses are divided into two groups-transforming and non-transforming RNA viruses. Transforming RNA viruses carry viral oncogenes that are homologous to the host oncogene, their expression in infected cells results in oncogenic transformation of the cell. Non-transforming RNA viruses induce oncogenesis similar to the DNA viruses. Contrary, oncolytic viruses selectively replicate in cancerous cells and induce cell death without any damage to the normal tissues. Typically, oncolytic viruses are nonpathogenic to humans that can naturally replicate in cancer cells by exploiting oncogenic cell signalling pathways. Pathogenic viruses can also be genetically manipulated which allow them to replicate in cancerous but not in normal cells. This review review describes the molecular mechanisms associated with virus induced oncogenesis and oncolysis.
    VL  - 7
    IS  - 3
    ER  - 

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Author Information
  • National Centre for Veterinary Type Cultures, ICAR-National Research Centre on Equines, Hisar, India

  • National Centre for Veterinary Type Cultures, ICAR-National Research Centre on Equines, Hisar, India

  • Department of Veterinary Microbiology and Biotechnology, Rajasthan University of Veterinary and Animal Sciences, Rajasthan, India

  • National Centre for Veterinary Type Cultures, ICAR-National Research Centre on Equines, Hisar, India

  • National Centre for Veterinary Type Cultures, ICAR-National Research Centre on Equines, Hisar, India

  • National Centre for Veterinary Type Cultures, ICAR-National Research Centre on Equines, Hisar, India

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