Article (Scientific journals)
The contribution of large genomic deletions at the CDKN2A locus to the burden of familial melanoma.
Lesueur, F.; de Lichy, M.; Barrois, M. et al.
2008In British Journal of Cancer, 99 (2), p. 364-70
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Keywords :
Aged; Aged, 80 and over; Base Sequence; Carrier Proteins/genetics; Chromosomes, Human, Pair 9; Cyclin-Dependent Kinase Inhibitor p16/genetics; Exons; Female; Gene Deletion; Genes, p16; Genetic Predisposition to Disease; Humans; Male; Melanoma/genetics; Middle Aged; Molecular Sequence Data; Pedigree; Point Mutation; Reverse Transcriptase Polymerase Chain Reaction; Tumor Suppressor Protein p14ARF/genetics
Abstract :
[en] Mutations in two genes encoding cell cycle regulatory proteins have been shown to cause familial cutaneous malignant melanoma (CMM). About 20% of melanoma-prone families bear a point mutation in the CDKN2A locus at 9p21, which encodes two unrelated proteins, p16(INK4a) and p14(ARF). Rare mutations in CDK4 have also been linked to the disease. Although the CDKN2A gene has been shown to be the major melanoma predisposing gene, there remains a significant proportion of melanoma kindreds linked to 9p21 in which germline mutations of CDKN2A have not been identified through direct exon sequencing. The purpose of this study was to assess the contribution of large rearrangements in CDKN2A to the disease in melanoma-prone families using multiplex ligation-dependent probe amplification. We examined 214 patients from independent pedigrees with at least two CMM cases. All had been tested for CDKN2A and CDK4 point mutation, and 47 were found positive. Among the remaining 167 negative patients, one carried a novel genomic deletion of CDKN2A exon 2. Overall, genomic deletions represented 2.1% of total mutations in this series (1 of 48), confirming that they explain a very small proportion of CMM susceptibility. In addition, we excluded a new gene on 9p21, KLHL9, as being a major CMM gene.
Disciplines :
Genetics & genetic processes
Author, co-author :
Lesueur, F.
de Lichy, M.
Barrois, M.
Durand, G.
Bombled, J.
Avril, M.-F.
Chompret, A.
Boitier, F.
Lenoir, G. M.
Bressac-de Paillerets, B.
Baccard, Monique
Bachollet, Bertrand
Berthet, Pascaline
Bonadona, Valerie
Bonnetblanc, Jean-Marie
Caron, Olivier
Chevrant-Breton, Jacqueline
Cuny, Jean-Francois
Dalle, Stephane
Delaunay, Michele
Demange, Liliane
De Quatrebarbes, Julie
Dore, Jean-Francois
Frenay, Marc
Fricker, Jean-Pierre
Gauthier-Villars, Marion
Gesta, Paul
Giraud, Sophie
Gorry, Philippe
Grange, Florent
Green, Andrew
Huiart, Laetitia
Janin, Nicolas ;  Institut Gustave Roussy - IGR - Villejuif - Paris > Oncologie Médicale
Joly, Pascal
Kerob, Delphine
Lasset, Christine
Leroux, Dominique
Limacher, Jean-Marc
Longy, Michel
Mansard, Sandrine
Marrou, Karine
Martin-Denavit, Tanguy
Mateus, Christine
Maubec, Eve
Olivier-Faivre, Laurence
Orlandini, Vincent
Pujol, Pascal
Sassolas, Bruno
Stoppa-Lyonnet, Dominique
Thomas, Luc
Vabres, Pierre
Venat, Laurence
Wierzbicka, Ewa
Zattara, Helene
More authors (44 more) Less
Language :
English
Title :
The contribution of large genomic deletions at the CDKN2A locus to the burden of familial melanoma.
Publication date :
2008
Journal title :
British Journal of Cancer
ISSN :
0007-0920
eISSN :
1532-1827
Publisher :
Nature Publishing Group, London, United Kingdom
Volume :
99
Issue :
2
Pages :
364-70
Peer reviewed :
Peer Reviewed verified by ORBi
Available on ORBi :
since 29 January 2009

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