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New mutations and protein variants of NBS1 are identified in cancer cell lines

✍ Scribed by Alessandra Tessitore; Leda Biordi; Vincenzo Flati; Elena Toniato; Paolo Marchetti; Enrico Ricevuto; Corrado Ficorella; Luigi Scotto; Giuseppe Giannini; Luigi Frati; Carlo Masciocchi; Vincenzo Tombolini; Alberto Gulino; Stefano Martinotti

Publisher
John Wiley and Sons
Year
2002
Tongue
English
Weight
336 KB
Volume
36
Category
Article
ISSN
1045-2257

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✦ Synopsis

Abstract

Alterations of the NBS1 gene are responsible for Nijmegen breakage syndrome (NBS), which is characterized by chromosomal instability, radiosensitivity, and cancer predisposition. NBS1 protein (Nibrin) is part of a molecular complex (NBS1– MRE11A–RAD50) that is functionally involved in DNA double‐strand–break repair. Defects in recombination or in repair mechanisms at the level of DNA breakage can lead to chromosomal aberrations, genetic instability, as well as cancer predisposition syndromes (i.e., NBS, ataxia‐telangiectasia, Bloom syndrome). In this study, we examined 20 cancer cell lines to evaluate the potential involvement of NBS1 in tumoral pathogenesis. Three different mutations, generating truncated or aberrant NBS1 transcripts, were identified at the level of NBS1 mRNA. In addition, two shorter NBS1 protein variants were detected in two cell lines. These data suggest a possible involvement of NBS1 in tumor development. Β© 2003 Wiley‐Liss, Inc.

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