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Titolo:
P53 MUTATION AS THE 2ND EVENT IN JUVENILE CHRONIC MYELOGENOUS LEUKEMIA IN A PATIENT WITH NEUROFIBROMATOSIS TYPE-1
Autore:
LURIA D; AVIGAD S; COHEN IJ; STARK B; WEITZ R; ZAIZOV R;
Indirizzi:
SCHNEIDER CHILDRENS MED CTR ISRAEL,CTR PEDIAT HEMATOL ONCOL IL-49202 PETAH TIQWA ISRAEL SCHNEIDER CHILDRENS MED CTR ISRAEL,CTR PEDIAT HEMATOL ONCOL IL-49202 PETAH TIQWA ISRAEL TEL AVIV UNIV,FELSENSTEIN MED RES CTR IL-69978 TEL AVIV ISRAEL TEL AVIV UNIV,SACKLER SCH MED IL-69978 TEL AVIV ISRAEL SCHNEIDER CHILDRENS MED CTR ISRAEL,CTR PEDIAT NEUROL IL-49202 PETAH TIQWA ISRAEL
Titolo Testata:
Cancer
fascicolo: 10, volume: 80, anno: 1997,
pagine: 2013 - 2018
SICI:
0008-543X(1997)80:10<2013:PMAT2E>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
MALIGNANT MYELOID DISORDERS; POLYMERASE CHAIN-REACTION; NF1 GENE; VONRECKLINGHAUSEN NEUROFIBROMATOSIS; REPEAT POLYMORPHISMS; CELL-LINES; GROWTH; NEUROBLASTOMA; DELETIONS; P21(RAS);
Keywords:
NEUROFIBROMATOSIS TYPE 1; P53; JUVENILE CHRONIC MYELOGENOUS LEUKEMIA; MUTATIONS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
41
Recensione:
Indirizzi per estratti:
Citazione:
D. Luria et al., "P53 MUTATION AS THE 2ND EVENT IN JUVENILE CHRONIC MYELOGENOUS LEUKEMIA IN A PATIENT WITH NEUROFIBROMATOSIS TYPE-1", Cancer, 80(10), 1997, pp. 2013-2018

Abstract

BACKGROUND. Young patients with neurofibromatosis type 1 (NF1) are atincreased risk of developing various malignancies, most of which are myeloid disorders. The observed loss of NF1 allele in the myeloid malignancies of NF1 patients suggests a role of NF1 as a tumor suppressor gene. Loss of 17p was found to be quite frequent in neural crest tumors from patients with NF1, raising the possibility of p53 tumor suppressor gene involvement in other NF1-related tumors.METHODS, The authors studied mutations in the NF1 and p53 genes, using loss of heterozygosity, single strand conformation polymorphism, heteroduplex and sequencing analyses. RESULTS. An NF1 germline mutation was identified in exon 31 of a child who developed juvenile chronic myelogenous leukemia (JCML). The mutation was segregated within the proband's family. A 14bp deletion at exon 6 of the p53 gene was observed when JCML was diagnosed,and the wild-type p53 allele was lost during progression of the disease. No loss of the normal NF1 allele could be detected. CONCLUSIONS, Agermline mutation in the NF1 gene and sequential inactivation of p53 alleles in the malignant clone of JCML raise the possibility of a correlation between NF1 and p53 genes in the tumorigenesis of JCML. (C) 1997 American Cancer Society.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 06:49:00