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Titolo:
Comparison of two human ovarian carcinoma cell lines (A2780/CP70 and MCAS)that are equally resistant to platinum, but differ at codon 118 of the ERCC1 gene
Autore:
Yu, JJ; Lee, KB; Mu, CJ; Li, QD; Abernathy, TV; Bostick-Bruton, F; Reed, E;
Indirizzi:
NCI, Med Ovarian Canc Sect, Dev Therapeut Dept, Med Branch,Div Clin Sci, Bethesda, MD 20892 USA NCI Bethesda MD USA 20892 Med Branch,Div Clin Sci, Bethesda, MD 20892 USA
Titolo Testata:
INTERNATIONAL JOURNAL OF ONCOLOGY
fascicolo: 3, volume: 16, anno: 2000,
pagine: 555 - 560
SICI:
1019-6439(200003)16:3<555:COTHOC>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
MESSENGER-RNA EXPRESSION; ACQUIRED CISPLATIN RESISTANCE; REPAIR EXCISION NUCLEASE; CANCER CELLS; DNA ADDUCT; TISSUES; P53; CHEMOTHERAPY; SENSITIVITY; MECHANISMS;
Keywords:
ERCC1; p53; DNA repair; cisplatin; ovarian cancer;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Reed, E NCI, Med Ovarian Canc Sect, Dev Therapeut Dept, Med Branch,Div Clin Sci, Bldg 10,Room 12N226, Bethesda, MD 20892 USA NCI Bldg 10,Room 12N226 Bethesda MD USA 20892 thesda, MD 20892 USA
Citazione:
J.J. Yu et al., "Comparison of two human ovarian carcinoma cell lines (A2780/CP70 and MCAS)that are equally resistant to platinum, but differ at codon 118 of the ERCC1 gene", INT J ONCOL, 16(3), 2000, pp. 555-560

Abstract

ERCC1 is an essential gene within the nucleotide excision repair process. We studied two human ovarian carcinoma cell lines for cisplatin resistance,which differed with respect to ERCC1. The A2780/CP70 cell line has been extensively studied previously, and has the wild-type ERCC1 sequence. The MCAS cell line has a recently described ERCC1 polymorphism at codon 118, whichis associated with an approximate 50% reduction in codon usage. These cells did not differ with respect to p53 sequence nor p53 mRNA induction following cisplatin exposure. The induction of ERCC1 mRNA was markedly reduced inMCAS cells as compared to A2780/CP70 cells. At the IC50 cisplatin dose foreach cell line, MCAS cells were less proficient at cisplatin-DNA adduct repair than A2780/CP70 cells. In absolute terms, A2780/CP70 cells repaired 3-fold as much adduct (2.7 pg/mu g DNA over 6 h vs 0.86 pg/mu g DNA); and when expressed in terms of the maximal DNA adduct load, A2780/CP70 cells repaired 50% more adduct than MCAS cells. MCAS cells had increased cytosolic inactivation of drug at the IC50 dose level, which has been previously suggested to be a compensatory cellular response for reduced DNA repair capacity. These data suggest the possibility that this specific ERCC1 polymorphism, may be associated with reduced DNA repair capacity in human ovarian cancer cells. This association may be effected through a reduction in peak production of ERCC1 mRNA, and a consequent reduction in the translation of ERCC1 mRNA into protein.

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Documento generato il 23/09/18 alle ore 08:05:13