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Titolo:
Mechanisms of resistance to imatinib (ST1571) and prospects for combination with conventional, chemotherapeutic agents
Autore:
Krystal, GW;
Indirizzi:
McGuire Dept Vet Affairs Med Ctr, Richmond, VA 23249 USA McGuire Dept Vet Affairs Med Ctr Richmond VA USA 23249 mond, VA 23249 USA Virginia Commonwealth Univ, Med Coll Virginia, Dept Med, Richmond, VA 23298 USA Virginia Commonwealth Univ Richmond VA USA 23298 , Richmond, VA 23298 USA
Titolo Testata:
DRUG RESISTANCE UPDATES
fascicolo: 1, volume: 4, anno: 2001,
pagine: 16 - 21
SICI:
1368-7646(200102)4:1<16:MORTI(>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
TYROSINE KINASE INHIBITOR; GROWTH-FACTOR RECEPTOR; CHRONIC MYELOGENOUS LEUKEMIA; ABL-POSITIVE CELLS; LUNG-CANCER GROWTH; BCR-ABL; C-KIT; IN-VIVO; 2-PHENYLAMINOPYRIMIDINE CLASS; ALPHA-1-ACID GLYCOPROTEIN;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Krystal, GW McGuire Dept Vet Affairs Med Ctr, 111K,1201 Broad Rock Blvd, Richmond, VA 23249 USA McGuire Dept Vet Affairs Med Ctr 111K,1201 Broad RockBlvd Richmond VA USA 23249
Citazione:
G.W. Krystal, "Mechanisms of resistance to imatinib (ST1571) and prospects for combination with conventional, chemotherapeutic agents", DRUG RESIST, 4(1), 2001, pp. 16-21

Abstract

Imatinib (ST157I,Glivec) is a small molecule drug selected for its abilityto inhibit the Bcr-Abl kinase, the pathogenic molecular abnormality in chronic myelogenous leukemia (CML), It also is an efficient inhibitor of the Kit and platelet-derived growth factor receptor tyrosine kinases, In vitro studies have demonstrated that this drug potently inhibits proliferation andinduces apoptosis of cells that depend on activation of these kinases. Phase I clinical studies have demonstrated remarkable activity against CML. However, these studies, as well as a variety of experimental models, have suggested that clinical resistance to ST157I could develop. The mechanisms forthe development of this resistance will be discussed along with the potential for circumventing ST157I resistance by combining it with traditional anti-neoplastic agents. (C) 2001 Harcourt Publishers Ltd.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 22:40:21