Journal article
Patients with chronic myeloid leukemia who maintain a complete molecular response after stopping imatinib treatment have evidence of persistent leukemia by DNA PCR
DM Ross, S Branford, JF Seymour, AP Schwarer, C Arthur, PA Bartley, C Slader, C Field, P Dang, RJ Filshie, AK Mills, AP Grigg, JV Melo, TP Hughes
Leukemia | Published : 2010
DOI: 10.1038/leu.2010.185
Abstract
Around 40-50% of patients with chronic myeloid leukemia (CML) who achieve a stable complete molecular response (CMR; undetectable breakpoint cluster region-Abelson leukemia gene human homolog 1 (BCR-ABL1) mRNA) on imatinib can stop therapy and remain in CMR, at least for several years. This raises the possibility that imatinib therapy may not need to be continued indefinitely in some CML patients. Two possible explanations for this observation are (1) CML has been eradicated or (2) residual leukemic cells fail to proliferate despite the absence of ongoing kinase inhibition. We used a highly sensitive patient-specific nested quantitative PCR to look for evidence of genomic BCR-ABL1 DNA in pat..
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Funding Acknowledgements
Professor Nicholas Cross and Dr Joannah Score (Wessex Regional Genetics Laboratory, Salisbury, United Kingdom) developed the original long-range PCR method for the detection of BCR-ABL1 genomic breakpoints. Dr John Reynolds, Ms Rachel Koelmeyer and Dr Ruth Columbus (Australasian Leukaemia & Lymphoma Group Trial Centre) contributed to the design of the clinical trial. Emeritus Professor Alexander Morley (Flinders University) provided advice on laboratory studies. This study was supported by research funding from Novartis Oncology to the Australasian Leukaemia & Lymphoma Group (clinical trial), and to the Institute of Medical & Veterinary Science, SA Pathology (laboratory studies).