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Titolo:
P16UV mutations in human skin epithelial tumors
Autore:
Soufir, N; Moles, JP; Vilmer, C; Moch, C; Verola, O; Rivet, J; Tesniere, A; Dubertret, L; Basset-Seguin, N;
Indirizzi:
Hop St Louis, Inst Rech Peau, INSERM, U312, F-75010 Paris, France Hop St Louis Paris France F-75010 u, INSERM, U312, F-75010 Paris, France IURC, Lab Dermatol Mol, Montpellier, France IURC Montpellier FranceIURC, Lab Dermatol Mol, Montpellier, France Hop St Louis, Serv Anatomopathol, Paris, France Hop St Louis Paris France p St Louis, Serv Anatomopathol, Paris, France
Titolo Testata:
ONCOGENE
fascicolo: 39, volume: 18, anno: 1999,
pagine: 5477 - 5481
SICI:
0950-9232(19990923)18:39<5477:PMIHSE>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
SQUAMOUS-CELL CARCINOMAS; P53 GENE-MUTATIONS; SUPPRESSOR GENE; INK4A LOCUS; ULTRAVIOLET-IRRADIATION; GERMLINE MUTATIONS; HUMAN CANCERS; CYCLE ARREST; CDKN2 GENE; MELANOMA;
Keywords:
INKA-ARF locus; p16 gene; p53 gene; Cdk4 gene; non melanoma skin cancers; tandem mutation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Basset-Seguin, N Hop St Louis, Inst Rech Peau, INSERM, U312, Pavillon Bazin,1 Ave Claude Vellefaux, F-75010 Paris, France Hop St Louis Pavillon Bazin,1 Ave Claude Vellefaux Paris France F-75010
Citazione:
N. Soufir et al., "P16UV mutations in human skin epithelial tumors", ONCOGENE, 18(39), 1999, pp. 5477-5481

Abstract

The p16 gene expresses two alternative transcripts (p16 alpha and p16 beta) involved in tumor suppression via the retinoblastoma (Rb) or p53 pathways. Disruption of these pathways can occur through inactivation of p16 or p53, or activating mutations of cyclin dependant kinase 4 gene (Cdk4). We searched for p16, Cdk4 and p53 gene mutations in 20 squamous cell carcinomas (SSCs), 1 actinic keratosis (AK), and 28 basal cell carcinomas (BCCs), using PCR-SSCP. A deletion and methylation analysis of p16 was also performed. Six different mutations (12%) were detected in exon 2 of p16 (common to p16 alpha and p16 beta), in five out of 21 squamous lesions (24%) (one AK and four SCCs) and one out of 28 BCCs (3.5%), These included four (66%) ultraviolet (UV)-type mutations (two tandems CC : GC to TT : AA transitions and two C : G to T : A transitions at dipyrimidic site) and two transversions, P53 mutations were present in 18 samples (37%), mostly of UV type. Of these, only two (one BCC and one AK) harboured simultaneously mutations of p16, but with no consequence on p16 beta transcript. Our data demonstrate for the first time the presence of p16 UV induced mutations in non melanoma skin cancer, particularly in the most aggressive SCC type, and support that p16 and p53 are involved in two independent pathways in skin carcinogenesis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 20:11:58