Varying response to escalating the dose of imatinib in patients with CML who "acquire" a BCR-ABLM244V mutant allele

Blood

Volumn 108, Issue 8, 2006, Pages 2881-2882

  Anand, Mona ^b   Khorashad, Jamshid ^b   Marin, David ^b   Apperley, Jane F ^b   Goldman, John M ^a   Kaeda, Jaspal Singh ^b  

^a IMPERIAL COLLEGE LONDON   (United Kingdom)

^b NONE

Author keywords

[No Author keywords available]

Indexed keywords

BCR ABL PROTEIN; IMATINIB; ANTINEOPLASTIC AGENT; PIPERAZINE DERIVATIVE; PYRIMIDINE DERIVATIVE;

CHRONIC MYELOID LEUKEMIA; DOSE RESPONSE; HUMAN; IC 50; LETTER; PRIORITY JOURNAL; REAL TIME POLYMERASE CHAIN REACTION; SINGLE NUCLEOTIDE POLYMORPHISM; DRUG RESISTANCE; GENETIC TRANSCRIPTION; GENETICS; ONCOGENE; POINT MUTATION; POLYMERASE CHAIN REACTION; TIME;

ANTINEOPLASTIC AGENTS; DOSE-RESPONSE RELATIONSHIP, DRUG; DRUG RESISTANCE, NEOPLASM; GENES, ABL; HUMANS; LEUKEMIA, MYELOID, CHRONIC; PIPERAZINES; POINT MUTATION; POLYMERASE CHAIN REACTION; PYRIMIDINES; TIME FACTORS; TRANSCRIPTION, GENETIC;

EID: 33750613947     PISSN: 00064971     EISSN: 00064971     Source Type: Journal    
DOI: 10.1182/blood-2006-05-020859     Document Type: Letter

References (4)

1. Azam M, Latek RR, Daley GQ. Mechanisms of autoinhibition and STI-571 imatinib resistance revealed by mutagenesis of BCR-ABL. Cell. 2003;112:737-740.
2. Branford S, Rudzki Z, Walsh S, et al. Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor prognosis. Blood. 2003;102:276-283.
3. Corbin AS, La Rosee P, Stroffregen EP, Druker BJ, Deininger MW. Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib. Blood. 2003;101:4611-4614.
4. Khorashad JS, Anand M, Marin D, et al. The presence of a BCR-ABL mutant allele in CML does not always explain clinical resistance to imatinib. Leukemia. 2006;20:658-663.