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Titolo:
CD95-mediated apoptosis of human glioma cells: Modulation by epidermal growth factor receptor activity
Autore:
Steinbach, JP; Supra, P; Huang, HJS; Cavenee, WK; Weller, M;
Indirizzi:
Univ Tubingen, Sch Med, Dept Neurol, Mol Neurooncol Lab, D-72076 Tubingen,Germany Univ Tubingen Tubingen Germany D-72076 col Lab, D-72076 Tubingen,Germany Ludwig Inst Canc Res, San Diego Branch, La Jolla, CA USA Ludwig Inst Canc Res La Jolla CA USA San Diego Branch, La Jolla, CA USA
Titolo Testata:
BRAIN PATHOLOGY
fascicolo: 1, volume: 12, anno: 2002,
pagine: 12 - 20
SICI:
1015-6305(200201)12:1<12:CAOHGC>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN-MALIGNANT GLIOMA; ANTIBODY-MEDIATED APOPTOSIS; HUMAN GLIOBLASTOMA CELLS; MONOCLONAL-ANTIBODY; TYROSINE KINASE; CD95L-INDUCED APOPTOSIS; BREAST-CANCER; GENE-TRANSFER; CD95 LIGAND; EXPRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Steinbach, JP Univ Tubingen, Sch Med, Dept Neurol, Mol Neurooncol Lab, Seyler Str 3, D-72076 Tubingen, Germany Univ Tubingen Seyler Str 3 Tubingen Germany D-72076 Germany
Citazione:
J.P. Steinbach et al., "CD95-mediated apoptosis of human glioma cells: Modulation by epidermal growth factor receptor activity", BRAIN PATH, 12(1), 2002, pp. 12-20

Abstract

The death ligands CD95L and Apo2L/TRAIL are promising investigational agents for the treatment of malignant glioma. EGFR is overexpressed in a significant proportion of malignant gliomas in vivo. Here, we report that CD95L-induced cell death is enhanced by EGFR inhibition using tyrphostine AG1478 in 7 of 12 human malignant glioma cell lines. Conversely, CD95-mediated and Apo2L-induced cell death are both inhibited by overexpression of EGFR in LN-229 cells. CD95L-induced cell death augmented by AG1478 is accompanied by enhanced processing of caspase 8. LN-229 cells overexpressing the viral caspase inhibitor, crm-A, are not sensitized to CD95L-induced cell death by AG1478, indicating that EGFR exerts its antiapoptotic properties through a caspase 8-dependent pathway. These data define a modulatory effect of EGFR-activity on death ligand-induced apoptosis and indicate that EGFR inhibition is likely to improve the efficacy of death ligand-based cancer therapies. Furthermore, it is tempting to speculate that EGFR amplification protects tumor cells from death ligand-mediated host immune responses in vivo and thatEGFR's effects on death receptor-mediated apoptosis may explain the anti-tumor effects of non-cytotoxic, unarmed anti-EGFR family antibodies.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/02/20 alle ore 02:44:17