Abstract：
:It is currently widely accepted that genetic instability is key to cancer development. Many types of cancers arise as a consequence of a gradual accumulation of nucleotide aberrations, each mutation conferring growth and/or survival advantage. Genetic instability could also proceed in sudden bursts leading to a more drastic upheaval of structure and organization of the genome. Genetic instability, as an operative force, will produce genetic variants and the greater the instability, the larger the number of variants. We report here that the overexpression of human DNA polymerase kappa, an error-prone enzyme that is up-regulated in lung cancers, induces DNA breaks and stimulates DNA exchanges as well as aneuploidy. Probably as the result of so many perturbations, excess polymerase kappa favors the proliferation of competent tumor cells as observed in immunodeficient mice. These data suggest that altered regulation of DNA metabolism might be related to cancer-associated genetic changes and phenotype.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Bavoux C,Leopoldino AM,Bergoglio V,O-Wang J,Ogi T,Bieth A,Judde JG,Pena SD,Poupon MF,Helleday T,Tagawa M,Machado C,Hoffmann JS,Cazaux Csubject
Has Abstractpub_date
2005-01-01 00:00:00pages
325-30issue
1eissn
0008-5472issn
1538-7445pii
65/1/325journal_volume
65pub_type
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