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Carcinogenesis Advance Access published online on February 20, 2006
Carcinogenesis, doi:10.1093/carcin/bgi356
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received December 12, 2005
Revised January 20, 2006
Accepted January 23, 2006

CARCINOGENESIS

Specific TP53 mutation pattern in radiation-induced sarcomas

Nathalie Gonin-Laurent 1, Anne Gibaud 1, Mathilde Huygue 1, Sandrine H. Lefèvre 1, Morgane Le Bras 2, Laurent Chauveinc 3, Xavier Sastre-Garau 4, François Doz 5, Livia Lumbroso 6, Sylvie Chevillard 7, and Bernard Malfoy 1 *

1 UMR7147 Institut Curie-CNRS-UPMC, CEA LRC38, Institut Curie, Paris, France
2 Génotoxicologie des Tumeurs, Institut Curie, Paris, France
3 Service de Radiothérapie, Institut Curie, Paris, France
4 Service de Pathologie, Institut Curie, Paris, France
5 Departement de Pédiatrie, Institut Curie, Paris, France
6 Service d'Ophtalmologie, Institut Curie, Paris, France
7 CEA, DSV DRR, Fontenay-aux-Roses, France

* To whom correspondence should be addressed.
Bernard Malfoy, E-mail: bernard.malfoy{at}curie.fr


  Abstract

The mutagenic properties of ionizing-radiation are well known, but the presence of specific mutations in human radiation-induced tumours is not established. We have studied a series of 36 secondary sarcomas arising in the irradiation field of a primary tumour following radiotherapy. The allelic status and the presence of mutations of the TP53 gene were investigated. The mutation pattern was compared with data from sporadic sarcomas recorded in the IARC TP53 somatic mutations database. A high proportion (58%) of the radiation-induced sarcomas exhibited a somatic inactivating mutation for one allele of TP53, systematically associated with a loss of the other allele. The high frequency (52%) of short deletions observed in the mutation pattern of radiation-induced sarcomas may be related to the induction of DNA breaks by ionizing radiation. The lack of hyper-reactivity of CpG dinucleotides and the presence of recurrent sites of mutation at codons 135 and 237 seem also to be specific for radiation-tumorigenesis.


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