Many BCR-ABL1 compound mutations reported in chronic myeloid leukemia patients may actually be artifacts due to PCR-mediated recombination
Open Access
- 3 July 2014
- journal article
- Published by American Society of Hematology in Blood
- Vol. 124 (1), 153-155
- https://doi.org/10.1182/blood-2014-05-573485
Abstract
No abstract availableKeywords
This publication has 10 references indexed in Scilit:
- Rapid identification of compound mutations in patients with Philadelphia-positive leukaemias by long-range next generation sequencingEuropean Journal Of Cancer, 2014
- Molecular dynamics reveal BCR-ABL1 polymutants as a unique mechanism of resistance to PAN-BCR-ABL1 kinase inhibitor therapyProceedings of the National Academy of Sciences of the United States of America, 2014
- Unraveling the complexity of tyrosine kinase inhibitor–resistant populations by ultra-deep sequencing of the BCR-ABL kinase domainBlood, 2013
- BCR-ABL1 compound mutations in tyrosine kinase inhibitor–resistant CML: frequency and clonal relationshipsBlood, 2013
- Sensitive Detection of BCR-ABL1 Mutations in Patients With Chronic Myeloid Leukemia After Imatinib Resistance Is Predictive of Outcome During Subsequent TherapyJournal of Clinical Oncology, 2011
- Targeting Bcr–Abl by combining allosteric with ATP-binding-site inhibitorsNature, 2010
- AP24534, a Pan-BCR-ABL Inhibitor for Chronic Myeloid Leukemia, Potently Inhibits the T315I Mutant and Overcomes Mutation-Based ResistanceCancer Cell, 2009
- Bias and artifacts in multitemplate polymerase chain reactions (PCR)Journal of Bioscience and Bioengineering, 2003
- Recombinant DNA sequences generated by PCR amplificationMolecular Biology and Evolution, 1997
- DNA recombination during PCRNucleic Acids Research, 1990