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
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