Unraveling the complexity of tyrosine kinase inhibitor–resistant populations by ultra-deep sequencing of the BCR-ABL kinase domain
Open Access
- 29 August 2013
- journal article
- Published by American Society of Hematology in Blood
- Vol. 122 (9), 1634-1648
- https://doi.org/10.1182/blood-2013-03-487728
Abstract
Key Points UDS demonstrated that BCR-ABL KD mutations detectable with conventional methods may just be the tip of the iceberg. The information provided by conventional Sanger sequencing may not always be sufficient to predict responsiveness to a given TKI.Keywords
This publication has 44 references indexed in Scilit:
- BCR-ABL1 compound mutations in tyrosine kinase inhibitor–resistant CML: frequency and clonal relationshipsBlood, 2013
- Ponatinib in Refractory Philadelphia Chromosome–Positive LeukemiasNew England Journal of Medicine, 2012
- Application of next-generation sequencing technologies in virologyJournal of General Virology, 2012
- Poor response to second-line kinase inhibitors in chronic myeloid leukemia patients with multiple low-level mutations, irrespective of their resistance profileBlood, 2012
- Detection of Minority Resistance during Early HIV-1 Infection: Natural Variation and Spurious Detection rather than Transmission and Evolution of Multiple Viral VariantsJournal of Virology, 2011
- A pyrosequencing-based test for detection and relative quantification of the BCR-ABL1 T315I point mutationJournal of Clinical Pathology, 2011
- AP24534, a Pan-BCR-ABL Inhibitor for Chronic Myeloid Leukemia, Potently Inhibits the T315I Mutant and Overcomes Mutation-Based ResistanceCancer Cell, 2009
- Next-generation DNA sequencingNature Biotechnology, 2008
- Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potencyJCI Insight, 2007
- A simple method for estimating evolutionary rates of base substitutions through comparative studies of nucleotide sequencesJournal of Molecular Evolution, 1980