Non-homologous End-joining Genes are not Inactivated in Human Radiation-induced Sarcomas with Genomic Instability | Zendy

Sandrine Lefevre | Zendy; Arnaud Coquelle | Zendy; Nathalie BritzenLaurent | Zendy; Andrej Cör | Zendy; Nicolas Vogt | Zendy; L. Chauveinc | Zendy; Philippe Anract | Zendy; Bernard Dutrillaux | Zendy; Sylvie Chevillard | Zendy; Bernard Malfoy | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Non-homologous End-joining Genes are not Inactivated in Human Radiation-induced Sarcomas with Genomic Instability

Author(s) -

Sandrine Lefevre,

Arnaud Coquelle,

Nathalie BritzenLaurent,

Andrej Cör,

Nicolas Vogt,

L. Chauveinc,

Philippe Anract,

Bernard Dutrillaux,

Sylvie Chevillard,

Bernard Malfoy

Publication year - 2005

Publication title -

journal of radiation research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.643

H-Index - 60

eISSN - 1349-9157

pISSN - 0449-3060

DOI - 10.1269/jrr.46.223

Subject(s) - genome instability , ku70 , ku80 , non homologous end joining , dna repair protein xrcc4 , biology , dna repair , rad50 , gene , loss of heterozygosity , homologous recombination , genetics , homologous chromosome , cancer research , genomic dna , dna , dna damage , allele , dna mismatch repair , dna binding protein , transcription factor

DNA double-strand break (DSB) repair pathways are implicated in the maintenance of genomic stability. However the alterations of these pathways, as may occur in human tumor cells with strong genomic instability, remain poorly characterized. We analyzed the loss of heterozygosity (LOH) and the presence of mutations for a series of genes implicated in DSB repair by non-homologous end-joining in five radiation-induced sarcomas devoid of both active Tp53 and Rb1. LOH was recurrently observed for 8 of the 9 studied genes (KU70, KU80, XRCC4, LIG4, Artemis, MRE11, RAD50, NBS1) but not for DNA-PKcs. No mutation was found in the remaining allele of the genes with LOH and the mRNA expression did not correlate with the allelic status. Our findings suggest that non-homologous end-joining repair pathway alteration is unlikely to be involved in the high genomic instability observed in these tumors.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research