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Titolo:
LOSS OF THE P16(INK4A) AND P15(INK4B) GENES, AS WELL AS NEIGHBORING 9P21 MARKERS, IN SPORADIC MELANOMA
Autore:
FLORES JF; WALKER GJ; GLENDENING JM; HALUSKA FG; CASTRESANA JS; RUBIO MP; PASTORFIDE GC; BOYER LA; KAO WH; BULYK ML; BARNHILL RL; HAYWARD NK; HOUSMAN DE; FOUNTAIN JW;
Indirizzi:
UNIV SO CALIF,DEPT BIOCHEM,INST MED GENET,2011 ZONAL AVE HMR413 LOS ANGELES CA 90033 UNIV SO CALIF,DEPT BIOCHEM & MOL BIOL,INST MED GENET LOS ANGELES CA 90033 QUEENSLAND INST MED RES BRISBANE QLD 4029 AUSTRALIA MASSACHUSETTS GEN HOSP,DEPT ONCOL BOSTON MA 02114 CSIC,INST INVEST BIOMED E-28029 MADRID SPAIN HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL BOSTON MA 02114 MIT,CTR CANC RES,DEPT BIOL CAMBRIDGE MA 02139 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT PATHOL BOSTON MA 02115
Titolo Testata:
Cancer research
fascicolo: 21, volume: 56, anno: 1996,
pagine: 5023 - 5032
SICI:
0008-5472(1996)56:21<5023:LOTPAP>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-SUPPRESSOR GENE; KINASE-4 INHIBITOR GENE; SQUAMOUS-CELL CARCINOMA; HOMOZYGOUS DELETIONS; FAMILIAL MELANOMA; CHROMOSOME 9P; MUTATIONAL ANALYSIS; MALIGNANT-MELANOMA; CYCLE INHIBITION; P16;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
58
Recensione:
Indirizzi per estratti:
Citazione:
J.F. Flores et al., "LOSS OF THE P16(INK4A) AND P15(INK4B) GENES, AS WELL AS NEIGHBORING 9P21 MARKERS, IN SPORADIC MELANOMA", Cancer research, 56(21), 1996, pp. 5023-5032

Abstract

Although homozygous deletions of the cyclin-dependent kinase inhibitor 2 gene p16(INK4a) on 9p21 have been reported frequently in metastatic melanoma cell lines, and intragenic mutations within the p16(INK4a) gene have been detected in familial melanoma kindreds, specific targeting of this gene in the development of sporadic melanoma in vivo remains controversial. Southern analyses were performed in this study to initially assess the frequency of hemi- or homozygous losses of p16(INK4a), as well as its neighboring family member, p15(INK4b) and other candidate regions within 9p21, in sporadic melanoma. Overall, 22 of 40 (55%) uncultured sporadic melanoma DNAs were determined to harbor deletions of 1-11 markers/genes located on 9p21. This included 10 tumors (25%; 10 of 40) with homozygous deletions limited to either the p16(INK4a) gene only (20%; 2 of 10), both the p16(INK4a) and p15(INK4b) genes (10%; 1 of 10), another novel 9p21 gene, FB19 (10%; 1 of 10), or all three of these genes plus surrounding markers (60%; 6 of 10). In subsequent single-strand conformation polymorphism and sequencing analyses, intragenic mutations in the p16(INK4a) gene were also revealed in two (10%; 2 of 21) melanoma DNAs that retained one copy of this locus. By comparison, the frequency of p16(INK4a) and p15(INK4b) homozygous deletions, as well as p16(INK4a) mutations, in melanoma cell lines (analyzed in parallel) was 2-3-fold higher at 61 (23 of 38) and 24% (9 of 38),respectively. These findings indicate that (a) p16(INK4a) is inactivated in vivo in over one-fourth (27.5%; 11 of 40) of sporadic melanomas; (b) mutation/deletion of p16(INK4a) may confer a selective growth advantage in vitro; and (c) other 9p21 tumor suppressor genes could be targeted during the development of melanoma.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 15:17:50