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Titolo:
E1A overcomes the apoptosis block in BCR-ABL plus leukemia cells and renders cells susceptible to induction of apoptosis by chemotherapeutic agents
Autore:
Stiewe, T; Parssanedjad, K; Esche, H; Opalka, B; Putzer, BM;
Indirizzi:
Univ Essen Gesamthsch, Sch Med, Inst Mol Biol Canc Res, D-45122 Essen, Germany Univ Essen Gesamthsch Essen Germany D-45122 Res, D-45122 Essen, Germany Univ Essen Gesamthsch, Sch Med, W German Canc Ctr, Dept Internal Med, D-45122 Essen, Germany Univ Essen Gesamthsch Essen Germany D-45122 Med, D-45122 Essen, Germany
Titolo Testata:
CANCER RESEARCH
fascicolo: 14, volume: 60, anno: 2000,
pagine: 3957 - 3964
SICI:
0008-5472(20000715)60:14<3957:EOTABI>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHRONIC MYELOGENOUS LEUKEMIA; BOX-BINDING FACTOR; CHRONIC MYELOID-LEUKEMIA; DNA-DAMAGING AGENTS; HUMAN CDC2 PROMOTER; ADENOVIRUS E1A; KINASE-ACTIVITY; P53-INDEPENDENT APOPTOSIS; RETINOBLASTOMA PROTEIN; HEMATOPOIETIC-CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
77
Recensione:
Indirizzi per estratti:
Indirizzo: Putzer, BM Univ Essen Gesamthsch, Sch Med, Inst Mol Biol, Hufelandstr 55, D-45122 Essen, Germany Univ Essen Gesamthsch Hufelandstr 55 Essen Germany D-45122 any
Citazione:
T. Stiewe et al., "E1A overcomes the apoptosis block in BCR-ABL plus leukemia cells and renders cells susceptible to induction of apoptosis by chemotherapeutic agents", CANCER RES, 60(14), 2000, pp. 3957-3964

Abstract

A crucial function of the BCR-ABL chimeric gene in chronic myeloid leukemia is the prolongation of cell survival by inhibition of apoptosis, BCR-ABL expression confers cross-resistance to multiple genotoxic anticancer drugs by inhibition of the apoptotic response to DNA damage in association with cell cycle arrest at the G(2)-M restriction point. Previous reports indicated that BCR-ABL exerts its antiapoptotic effect against various apoptotic stimuli upstream to the cleavage and activity of caspase-3, Here we shoe thatthe adenovirus E1A protein induces substantial apoptosis in BCR-ABL expressing K562 and LAMA-84 leukemia cells. This apoptotic activity of E1A is accompanied by processing of caspase-3 and cleavage of poly(ADP-ribose) polymerase and ran be significantly blocked by z-VAD-fmk Z-Val-Ala-Asp(OCH3)-CH2Fand the caspase-3-specific inhibitor Z-DEVD-FMK Z-Asp(OCH3)-Glu-Val-Asp(OCH3)-CH2F. Moreover, E1A renders K562 cells, which are particularly resistant to cell death irrespective of the inducing agent, susceptible to induction of apoptosis by the chemotherapeutic agents etoposide and daunorubicin. Counteracting the DNA damage-induced inactivation of cdc2 kinase, E1A reverses the drug-induced G(2)-M arrest. These results indicate that solitary delivery of E1A significantly antagonizes BCR-ABL-induced antiapoptotic functions and circumvents the inherent resistance to DNA damage-induced apoptosis, supporting the use of E1A in combination with chemotherapeutic agents as a promising therapeutic strategy for successful treatment of Philadelphia chromosome-positive leukemia in vivo.

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Documento generato il 08/07/20 alle ore 07:47:09