Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 22, Pages -Publisher
MDPI
DOI: 10.3390/ijms222212254
Keywords
genomic instability; chromosomal instability (CIN); microsatellite instability (MSI); homologous recombination (HR); non-homologous end-joining (NHEJ); microhomology-mediated end-joining (MMEJ); nucleotide excision repair (NER); mismatch repair (MMR)
Funding
- Uehara Memorial Foundation
- JSPS Kakenhi [21K12252]
- Grants-in-Aid for Scientific Research [21K12252] Funding Source: KAKEN
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Genomic instability contributes to cancer development, with repair defects increasing cancer risk. While many cancers develop independently of DNA repair defects, DNA repair systems are crucial for cell survival. Some cancers may compensate for deficiencies in one repair pathway by upregulating other pathways.
Many cancers develop as a consequence of genomic instability, which induces genomic rearrangements and nucleotide mutations. Failure to correct DNA damage in DNA repair defective cells, such as in BRCA1 and BRCA2 mutated backgrounds, is directly associated with increased cancer risk. Genomic rearrangement is generally a consequence of erroneous repair of DNA double-strand breaks (DSBs), though paradoxically, many cancers develop in the absence of DNA repair defects. DNA repair systems are essential for cell survival, and in cancers deficient in one repair pathway, other pathways can become upregulated. In this review, we examine the current literature on genomic alterations in cancer cells and the association between these alterations and DNA repair pathway inactivation and upregulation.
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