Molecular studies in chronic myeloid leukemia patients treated with tyrosine kinase inhibitors

Seminars in Hematology

Volumn 38, Issue 3 SUPPL. 8, 2001, Pages 15-21

  Sawyers, Charles L ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BCR ABL PROTEIN; IMATINIB; PROTEIN TYROSINE KINASE INHIBITOR; UNCLASSIFIED DRUG;

CHRONIC MYELOID LEUKEMIA; CLINICAL TRIAL; CYTOGENETICS; DRUG EFFICACY; ENZYME ACTIVITY; FLUORESCENCE IN SITU HYBRIDIZATION; HEMATOPOIETIC STEM CELL; HUMAN; IN VITRO STUDY; MOLECULAR BIOLOGY; PHILADELPHIA 1 CHROMOSOME; PRIORITY JOURNAL; QUANTITATIVE ASSAY; RELAPSE; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; REVIEW; SIGNAL TRANSDUCTION;

EID: 0034861220     PISSN: 00371963     EISSN: None     Source Type: Journal    
DOI: 10.1016/s0037-1963(01)90113-1     Document Type: Review

References (17)

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2. The biology of chronic myeloid leukemia
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5. Activity of a specific inhibitor of the Bcr-Abl tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the Philadelphia Chromosome
6. PCR-negative molecular remissions in chronic-, accelerated-, and blast crisis-phase CML patients treated with STI571. An Abl-specific kinase inhibitor
7. Monitoring minimal residual disease by Bcr-Abl Western and quantitative competitive RT-PCR in Philadelphia chromosome (Ph)-positive chronic myelogenous leukemia (CMR) on STI571 therapy
8. + leukemic cells to the Abl inhibitor STI 571
9. The tyrosine kinase inhibitor CGP57148B selectively inhibits the growth of BCR-ABL-positive cells
10. Selection and characterization of BCR-ABL positive cell lines with differential sensitivity to the tyrosine kinase inhibitor STI571: Diverse mechanisms of resistance
11. Induction of resistance to the Abelson inhibitor STI 571 in human leukemic cells through gene amplification
12. Mechanism of resistance to the ABL tyrosine kinase inhibitor STI571 in BCR/ ABL-transformed hematopoietic cell lines
13. Clinical resistance to STI-571 cancer therapy caused by BCRABL gene mutation or amplification
14. STI571 administered to chronic myeloid leukemia (CML) patients inhibits cell proliferation, induces apoptosis and initially causes partial inhibition of Bcr/Abl autophosphorylation
15. Detection of resistance to STI571 in patients with Bcr-Abl positive acute leukemia and chronic myeloid leukemia (CML) blast crisis
16. + leukemia patients treated with an Abl-specific kinase inhibitor is associated with reactivation of Bcr-Abl
17. BCR/ABL gene amplification: A possible mechanism of drug resistance in patients treated with an Abl-specific kinase inhibitor