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Titolo:
Bcl-2 expression in F-MuLV-induced erythroleukemias: a role for the anti-apoptotic action of Bcl-2 during tumor progression
Autore:
Howard, JC; Li, Q; Chu, W; Zochodne, B; Kapoor, M; Ung, Y; Rosen, K; Ben-David, Y;
Indirizzi:
Univ Toronto, Sunnybrook & Womens Coll, Hlth Sci Ctr, Dept Med Biophys,DivCanc Biol, Toronto, ON M4N 3M5, Canada Univ Toronto Toronto ON Canada M4N 3M5 Biol, Toronto, ON M4N 3M5, Canada Toronto Sunnybrook Reg Canc Ctr, Toronto, ON M4N 3M5, Canada Toronto Sunnybrook Reg Canc Ctr Toronto ON Canada M4N 3M5 M4N 3M5, Canada
Titolo Testata:
ONCOGENE
fascicolo: 18, volume: 20, anno: 2001,
pagine: 2291 - 2300
SICI:
0950-9232(20010426)20:18<2291:BEIFEA>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
MURINE LEUKEMIA-VIRUS; GROWTH-FACTOR INDEPENDENCE; CELLULAR P53 GENE; FRIEND-VIRUS; HEMATOPOIETIC MALIGNANCIES; CHROMOSOMAL BREAKPOINT; TOPOISOMERASE-II; IN-VITRO; B-CELLS; C-MYC;
Keywords:
Friend erythroleukemia; Bcl-2; p53; tumor progression;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
60
Recensione:
Indirizzi per estratti:
Indirizzo: Ben-David, Y Univ Toronto, Sunnybrook & Womens Coll, Hlth Sci Ctr, Dept Med Biophys,DivCanc Biol, 2075 Bayview Ave,Room S216, Toronto, ON M4N 3M5, Canada Univ Toronto 2075 Bayview Ave,Room S216 Toronto ON Canada M4N 3M5
Citazione:
J.C. Howard et al., "Bcl-2 expression in F-MuLV-induced erythroleukemias: a role for the anti-apoptotic action of Bcl-2 during tumor progression", ONCOGENE, 20(18), 2001, pp. 2291-2300

Abstract

Erythroleukemias induced by various strains of Friend virus are multistagemalignancies that result from the accumulation of genetic mutations, including the activation of proto-oncogenes and the inactivation of tumor suppressor genes. in this study, we demonstrate that Bcl-2 expression is activated in the majority of F-MuLV-induced erythroleukemia cell lines. In contrast, Bcl-2 was not expressed in any of the FV-P-induced erythroleukemia cell lines and protein levels were low or negligible in FV-A-induced erythroleukemia cell lines examined. In vivo, Bcl-2 expression levels gradually increased in F-MuLV-induced erythroleukemic cells prior to adaptation to culture. High expression of Bcl-2 in F-MuLV-induced erythroleukemic cells was shown to proceed the emergence of p53 mutation suggesting that Bcl-2 expression may delay p53 mutation in the leukemic cells, This is further supported by the demonstration that the majority of F-MuLV-induced erythroleukemia cell lines established from primary tumors induced in p53 mutant mice express lowto negligible levels of Bcl-2, We have shown that the high levels of Bcl-2expression in FV-P-induced erythroleukemic cells inhibited apoptosis induced by etoposide, low serum and p53 expression. Similarly, ectopic Bcl-2 expression within these cells also provided protection from apoptosis induced by etoposide and growth in low serum. These results suggest that the anti-apoptotic action of Bcl-2 may confer a selective in vivo and in vitro growthadvantage to F-MuLV-induced erythroleukemic cells, which is not shared by FV-P/ FV-A-induced erythroleukemic cells. The observed induction of Bcl-2 expression in vivo constitutes a novel but late oncogenic event associated with the progression of F-MuLV-induced erythroleukemias.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 19:26:12