Abstract
DNA damage usually happens in all cell types, which may originate from endogenous sources (i.e., DNA replication errors) or be emanated from radiations or chemicals. These damages range from changes in few nucleotides to significant structural abnormalities on chromosomes and, if not repaired, could disturb the cellular homeostasis or cause cell death. As the most significant response to DNA damage, DNA repair provides biological pathways by which DNA damages are corrected and returned into their natural circumstance. However, an aberration in the DNA repair mechanisms may result in genomic and chromosomal instability and the accumulation of mutations. The activation of oncogenes and/or inactivation of tumor suppressor genes is a serious consequence of genomic and chromosomal instability and may bring the cells into a cancerous phenotype. Therefore, genomic and chromosomal instability is usually considered a crucial factor in carcinogenesis and an important hallmark of various human malignancies. In the present study, we review our current understanding of the most updated mechanisms underlying genomic instability in cancer and discuss the potential promises of these mechanisms in finding new targets for the treatment of cancer.
Keywords: Genomic instability, chromosomal instability, DNA replication, DNA repair, oncogene, tumor suppressor gene, cancer, molecular mechanisms.
Current Pharmaceutical Design
Title:Genomic Instability in Cancer: Molecular Mechanisms and Therapeutic Potentials
Volume: 27 Issue: 28
Author(s): Arash Salmaninejad, Khandan Ilkhani, Havva Marzban, Jamshid G. Navashenaq, Samira Rahimirad, Fatemeh Radnia, Meysam Yousefi, Zahra Bahmanpour, Sara Azhdari and Amirhossein Sahebkar*
Affiliation:
- Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad,Iran
Keywords: Genomic instability, chromosomal instability, DNA replication, DNA repair, oncogene, tumor suppressor gene, cancer, molecular mechanisms.
Abstract: DNA damage usually happens in all cell types, which may originate from endogenous sources (i.e., DNA replication errors) or be emanated from radiations or chemicals. These damages range from changes in few nucleotides to significant structural abnormalities on chromosomes and, if not repaired, could disturb the cellular homeostasis or cause cell death. As the most significant response to DNA damage, DNA repair provides biological pathways by which DNA damages are corrected and returned into their natural circumstance. However, an aberration in the DNA repair mechanisms may result in genomic and chromosomal instability and the accumulation of mutations. The activation of oncogenes and/or inactivation of tumor suppressor genes is a serious consequence of genomic and chromosomal instability and may bring the cells into a cancerous phenotype. Therefore, genomic and chromosomal instability is usually considered a crucial factor in carcinogenesis and an important hallmark of various human malignancies. In the present study, we review our current understanding of the most updated mechanisms underlying genomic instability in cancer and discuss the potential promises of these mechanisms in finding new targets for the treatment of cancer.
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Cite this article as:
Salmaninejad Arash , Ilkhani Khandan , Marzban Havva , Navashenaq G. Jamshid , Rahimirad Samira , Radnia Fatemeh , Yousefi Meysam , Bahmanpour Zahra , Azhdari Sara and Sahebkar Amirhossein *, Genomic Instability in Cancer: Molecular Mechanisms and Therapeutic Potentials, Current Pharmaceutical Design 2021; 27 (28) . https://dx.doi.org/10.2174/1381612827666210426100206
DOI https://dx.doi.org/10.2174/1381612827666210426100206 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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