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Titolo:
p53 mutation and epidermal growth factor receptor overexpression in glioblastoma
Autore:
Yoon, KS; Lee, MC; Kang, SS; Kim, JH; Jung, S; Kim, YJ; Lee, JH; Ahn, KY; Lee, JS; Cheon, JY;
Indirizzi:
Chonnam Natl Univ, Sch Med, Dept Neurosurg, Kwangju 500757, South Korea Chonnam Natl Univ Kwangju South Korea 500757 Kwangju 500757, South Korea Res Inst Med Sci, Kwangju, South Korea Res Inst Med Sci Kwangju South Korea Inst Med Sci, Kwangju, South Korea Seonam Univ, Coll Med, Dept Pathol, Kwangju, South Korea Seonam Univ Kwangju South Korea Med, Dept Pathol, Kwangju, South Korea Ewha Womans Univ, Coll Nat Sci, Dept Pathol, Seoul 120750, South Korea Ewha Womans Univ Seoul South Korea 120750 hol, Seoul 120750, South Korea
Titolo Testata:
JOURNAL OF KOREAN MEDICAL SCIENCE
fascicolo: 4, volume: 16, anno: 2001,
pagine: 481 - 488
SICI:
1011-8934(200108)16:4<481:PMAEGF>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
MOLECULAR-GENETIC-ANALYSIS; SECONDARY GLIOBLASTOMAS; HUMAN GLIOMAS; BRAIN-TUMORS; OLIGODENDROGLIAL TUMORS; NEUROECTODERMAL TUMORS; HUMAN ASTROCYTOMAS; EGF RECEPTOR; TP53 GENE; DE-NOVO;
Keywords:
glioblastoma; protein, p53; receptor, epidermal growth factor; immunohistochemistry;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Lee, MC Chonnam Natl Univ Med Sch & Hosp, Dept Pathol, Dong Gu, 5 Hak Dong, Kwangju 501190, South Korea Chonnam Natl Univ Med Sch & Hosp 5 Hak Dong Kwangju South Korea 501190
Citazione:
K.S. Yoon et al., "p53 mutation and epidermal growth factor receptor overexpression in glioblastoma", J KOR MED S, 16(4), 2001, pp. 481-488

Abstract

Recent molecular studies indicate two different genetic pathways leading to the development of glioblastoma; final progression of astrocytoma and de novo formation. To define the mutual relationships of cytogenetic changes in the pathogenesis of glioblastoma, molecular histopathologic alterations of p53 and epidermal growth factor receptor (EGFR) were evaluated by single stranded conformational polymorphion, reverse transcriptase-polymerase chain reaction and immunohistochemical stains in 15 primary and 21 secondary glioblastomas. Mutations in p53 gene and positive immunoreactivity to p53 protein (DO1) were more prevalent in secondary glioblastomas than in primary glioblastomas. A correlation between p53 mutations and p53 immunopositivities in glioblastomas was observed in 83.3% of the cases. All cases with positive p53 immunoreactivities showed p53 mutations; however, 13.9% of glioblastomas with p53 immunopositivities lacked the relevant mutations, EGFR amplifications were detected in 73.3% of primary glioblastomas and 9.5% of secondary glioblastomas (p <0.001). The concurrence of p53 mutation and EGFR amplification was revealed in only 2 out of 15 primary glioblastomas and none among the secondary glioblastomas. Immunoreactivities for EGFR were noted in 66.7% of primary glioblastomas and in 9.5% of secondary glioblastomas (p <0.001). A correlation between EGFR amplification and EGFR immunopositivityin glioblastomas was observed in 91.7% of the cases. These data indicate that EGFR amplification and p53 mutations are two independent genetic eventsin the development of glioblastomas.

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Documento generato il 29/10/20 alle ore 21:39:48