Genome instability: a mechanistic view of its causes and consequences

By A. Aguilera, Belén Gómez‐González. Nature reviews genetics, 2008

817 citations recorded by the source corpus.

Subfields: Cell Biology, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/161ecd1ceb5ed1bf2b6e54804698ee871a29a07c

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Citations in the corpus

53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress (2011, background): “Apart from environmental genotoxic assaults, DNA can be damaged by errors during DNA replicatio”
Nuclear Receptor-Induced Chromosomal Proximity and DNA Breaks Underlie Specific Translocations in Cancer (2009, neutral): “Although it is well established that transcriptionally active regions, such as promoters, can be particularly susceptible to DNA damage ( Aguilera and Gomez-Gonzalez, 2008; Thomas and Rothstein, 1989), a prevalent view has been that tumor translocations may initially result from random chromosome r”
Maintaining genome stability at the replication fork (2010, background): “Genetic mutations that affect enzymes involved in replication result in an accumulation of DNA intermediates that trigger recombination and genome instabilit”
Cell cycle, CDKs and cancer: a changing paradigm (2009, background): “In addition, cells are exposed to exogenous and endogenous insults that can induce small mutations as well as gross chromosomal rearrangement”
R-loop formation is a distinctive characteristic of unmethylated human CpG island promoters (2012, neutral): “More broadly, a number of proteins involved in mRNA capping, spliceosome assembly, RNA splicing, mRNA surveillance, and mRNA export, contribute to regulating R loop formation (Aguilera and Gómez-González, 2008; Li and Manley, 2006; Paulsen et al., 2009), suggesting that R loop formationmay be mechan”
Androgen-induced TOP2B mediated double strand breaks and prostate cancer gene rearrangements (2010, background): “Finally, we speculate that the TIN model might underlie some of the genomic instability and copy number alterations observed during cancer progressio”
R loops: from transcription byproducts to threats to genome stability. (2012, background): “Yeast THO and THSC/TREX-2 R loop-forming mutants show a transcription-associated hyperrecombination phenotype and elevated chromosome and plasmid loss (reviewed in Aguilera and Gómez-González, 2008).”
Living on a break: cellular senescence as a DNA-damage response (2008, neutral): “The observation of a selective pressure in somatic cells for the inactivation of DDR genes during cancer progression is consistent with known cancer predisposition in patients and mouse models that carry germline mutations which impair DDR gene function”