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Titolo:
Chromosome 21 abnormalities with AMLI amplification in acute lymphoblasticleukemia
Autore:
Busson-Le Coniat, M; Khac, FN; Daniel, MT; Bernard, OA; Berger, R;
Indirizzi:
INSERM U434, CNRS SD 434, Paris, France INSERM U434 Paris FranceINSERM U434, CNRS SD 434, Paris, France Fdn Jean Dausset, Paris, France Fdn Jean Dausset Paris FranceFdn Jean Dausset, Paris, France Hop St Louis, Cent Hematol Lab, Paris, France Hop St Louis Paris FranceHop St Louis, Cent Hematol Lab, Paris, France
Titolo Testata:
GENES CHROMOSOMES & CANCER
fascicolo: 3, volume: 32, anno: 2001,
pagine: 244 - 249
SICI:
1045-2257(200111)32:3<244:C2AWAA>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE MYELOID-LEUKEMIA; AML1/PEBP2-ALPHA-B GENE; POINT MUTATIONS; DOWN-SYNDROME; RUNT DOMAIN; DELETIONS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
15
Recensione:
Indirizzi per estratti:
Indirizzo: Berger, R IGM, U 434,27 Rue Juliette Dodu, F-75010 Paris, France IGM U 434,27 Rue Juliette Dodu Paris France F-75010 ris, France
Citazione:
M. Busson-Le Coniat et al., "Chromosome 21 abnormalities with AMLI amplification in acute lymphoblasticleukemia", GENE CHROM, 32(3), 2001, pp. 244-249

Abstract

Fluorescence in situ. hybridization (FISH) studies were performed in threecases of acute lymphoblastic leukemia (ALL), with marker chromosomes to analyze the contribution of chromosome 21 in these markers. FISH with a chromosome 21 painting probe confirmed that chromosome 21 was involved in all three cases. FISH with YAC probes showed that the number of extra copies varied according to their location on chromosome 21. Attention was focused on the AML 1 gene, which was present as five copies in most of the cells exhibiting the marker chromosomes. As controls, 11 cases of childhood ALL were studied with PAC probes covering AML1. The results agreed with the banded karyotypes in 10 patients. FISH uncovered a clone with four copies of AML1 which were only observed by FISH analysis of interphase nuclei in one patient. No point mutation was detected in exons 3-5, encoding the runt domain of AML1 in the three cases, suggesting an oncogenic role of wild-type AML1 amplification. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/20 alle ore 10:31:10