We are analyzing https://link.springer.com/article/10.1186/s40169-016-0128-z.

Title:
Choices have consequences: the nexus between DNA repair pathways and genomic instability in cancer | Clinical and Translational Medicine
Description:
Background The genome is under constant assault from a multitude of sources that can lead to the formation of DNA double-stand breaks (DSBs). DSBs are cytotoxic lesions, which if left unrepaired could lead to genomic instability, cancer and even cell death. However, erroneous repair of DSBs can lead to chromosomal rearrangements and loss of heterozygosity, which in turn can also cause cancer and cell death. Hence, although the repair of DSBs is crucial for the maintenance of genome integrity the process of repair need to be well regulated and closely monitored. Main body The two most commonly used pathways to repair DSBs in higher eukaryotes include non-homologous end joining (NHEJ) and homologous recombination (HR). NHEJ is considered to be error-prone, intrinsically mutagenic quick fix remedy to seal together the broken DNA ends and restart replication. In contrast, HR is a high-fidelity process that has been very well conserved from phage to humans. Here we review HR and its sub-pathways. We discuss what factors determine the sub pathway choice including etiology of the DSB, chromatin structure at the break site, processing of the DSBs and the mechanisms regulating the sub-pathway choice. We also elaborate on the potential of targeting HR genes for cancer therapy and anticancer strategies. Conclusion The DNA repair field is a vibrant one, and the stage is ripe for scrutinizing the potential treatment efficacy and future clinical applications of the pharmacological inhibitors of HR enzymes as mono- or combinatorial therapy regimes.
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Keywords {🔍}

dna, pubmed, repair, article, google, scholar, cas, recombination, rad, central, homologous, pathway, cancer, cell, end, doublestrand, dsbs, break, cells, replication, strand, genome, formation, dsbr, inhibitors, nhej, pathways, breaks, dsb, yeast, biol, ends, ssdna, rna, nature, joining, junction, genes, fig, res, chromosomal, proteins, template, resection, information, damage, protein, helicases, gene, brca,

Topics {✒️}

double-strand-break repair model dna double-strand breaks double-strand dna breaks end-resection exposes micro-homologies double-strand break repair chromosomal double-strand breaks dna double-stand breaks double-strand breaks article download pdf double-strand break synthesis-dependent strand annealing rad51-mediated strand invasion double-holliday junction transition dna-dependent protein kinase dna-pk-independent fashion reactive oxygen species dna-dependent dsbr works atp-hydrolyzing activity coupled accelerate rad51-mediated displacement microhomology-mediated end joining rna-templated dna repair triggering recombination-mediated replication genomic instability dna damage checkpoint cell cycle-dependent repair cold spring harbor dna damage response rna-templated dsbr mediated mediate large-scale rearrangements dna damage tolerance control dna-end resection repair dsdna breaks error-free dsbr pathway alternative end-joining mechanisms genome editing his3 reporter gene article bhattacharjee cdk1-dependent phosphorylation nonhomologous end joining atp-dependent manner dna helicase deficiencies single-strand annealing end processing enzymes catalyzes strand invasion invading strand accompanied double holliday junction symmetrically related strand homologous strand pairing privacy choices/manage cookies junction resolving enzymes

Questions {❓}

Sfeir A, Symington LS (2015) Microhomology-mediated end joining: a back-up survival mechanism or dedicated pathway?

Schema {🗺️}

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      headline:Choices have consequences: the nexus between DNA repair pathways and genomic instability in cancer
      description:The genome is under constant assault from a multitude of sources that can lead to the formation of DNA double-stand breaks (DSBs). DSBs are cytotoxic lesions, which if left unrepaired could lead to genomic instability, cancer and even cell death. However, erroneous repair of DSBs can lead to chromosomal rearrangements and loss of heterozygosity, which in turn can also cause cancer and cell death. Hence, although the repair of DSBs is crucial for the maintenance of genome integrity the process of repair need to be well regulated and closely monitored. The two most commonly used pathways to repair DSBs in higher eukaryotes include non-homologous end joining (NHEJ) and homologous recombination (HR). NHEJ is considered to be error-prone, intrinsically mutagenic quick fix remedy to seal together the broken DNA ends and restart replication. In contrast, HR is a high-fidelity process that has been very well conserved from phage to humans. Here we review HR and its sub-pathways. We discuss what factors determine the sub pathway choice including etiology of the DSB, chromatin structure at the break site, processing of the DSBs and the mechanisms regulating the sub-pathway choice. We also elaborate on the potential of targeting HR genes for cancer therapy and anticancer strategies. The DNA repair field is a vibrant one, and the stage is ripe for scrutinizing the potential treatment efficacy and future clinical applications of the pharmacological inhibitors of HR enzymes as mono- or combinatorial therapy regimes.
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         general
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