ArticleOncotarget2016
Next-generation sequencing for sensitive detection of BCR-ABL1 mutations relevant to tyrosine kinase inhibitor choice in imatinib-resistant patients.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 58 citations in OpenAlex.
- Prediction of Response to FDA-Approved Targeted Therapy and Immunotherapy in Acute Lymphoblastic Leukemia (ALL).Current treatment options in oncology · 2024Review
- Validation of a novel NGS based BCR::ABL1 kinase domain mutation detection assay in Indian cohort.Scientific reports · 2024Article
- Mutation analysis of BCR-ABL1 kinase domain in chronic myeloid leukemia patients with tyrosine kinase inhibitors resistance: a Malaysian cohort study.BMC research notes · 2024Article
- Screening and Activity Evaluation of Novel BCR-ABL/T315I Tyrosine Kinase Inhibitors.Current medicinal chemistry · 2024Article
- Genetic Landscape of Chronic Myeloid Leukemia and a Novel Targeted Drug for Overcoming Resistance.International journal of molecular sciences · 2023Review
- A customized mass array panel forJournal of mass spectrometry and advances in the clinical lab · 2023Article
- Article
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- PROTAC: targeted drug strategy. Principles and limitations.Russian chemical bulletin = Izvestiia Akademii nauk. Seriia khimicheskaia · 2022Review
- Overcoming Resistance to Kinase Inhibitors: The Paradigm of Chronic Myeloid Leukemia.OncoTargets and therapy · 2022Review
- Genetic Landscape of Myeloproliferative Neoplasms with an Emphasis on Molecular Diagnostic Laboratory Testing.Life (Basel, Switzerland) · 2021Review
- Sensitivity and reliability of DNA-based mutation analysis by allele-specific digital PCR to follow resistant BCR-ABL1-positive cells.Leukemia · 2021Article
- Article
- Molecular Testing in CML between Old and New Methods: Are We at a Turning Point?Journal of clinical medicine · 2020Review
- A genome-scale CRISPR knock-out screen in chronic myeloid leukemia identifies novel drug resistance mechanisms along with intrinsic apoptosis and MAPK signaling.Cancer medicine · 2020Article
- Expert opinion-management of chronic myeloid leukemia after resistance to second-generation tyrosine kinase inhibitors.Leukemia · 2020Review
- Next-generation sequencing for BCR-ABL1 kinase domain mutations in adult patients with Philadelphia chromosome-positive acute lymphoblastic leukemia: A position paper.Cancer medicine · 2020Review
- Monitoring of Minimal Residual Disease (MRD) in Chronic Myeloid Leukemia: Recent Advances.Cancer management and research · 2020Review
- Nanopore Sequencing in Blood Diseases: A Wide Range of Opportunities.Frontiers in genetics · 2020Review
- Managing chronic myeloid leukemia for treatment-free remission: a proposal from the GIMEMA CML WP.Blood advances · 2019Article
Corrections and comments
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Authors and funding
18 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In chronic myeloid leukemia (CML) and Philadelphia-positive (Ph+) acute lymphoblastic leukemia (ALL) patients who fail imatinib treatment, BCR-ABL1 mutation profiling by Sanger sequencing (SS) is recommended before changing therapy since detection of specific mutations influences second-generation tyrosine kinase inhibitor (2GTKI) choice. We aimed to assess i) in how many patients who relapse on second-line 2GTKI therapy next generation sequencing (NGS) may track resistant mutations back to the sample collected at the time of imatinib resistance, before 2GTKI start (switchover sample) and ii) whether low level mutations identified by NGS always undergo clonal expansion. To this purpose, we used NGS to retrospectively analyze 60 imatinib-resistant patients (CML, n = 45; Ph+ ALL,n = 15) who had failed second-line 2GTKI therapy and had acquired BCR-ABL1 mutations (Group 1) and 25 imatinib-resistant patients (CML, n = 21; Ph+ ALL, n = 4) who had responded to second-line 2GTKI therapy, for comparison (Group 2). NGS uncovered that in 26 (43%) patients in Group 1, the 2GTKI-resistant mutations that triggered relapse were already detectable at low levels in the switchover sample (median mutation burden, 5%; range 1.1%-18.4%). Importantly, none of the low level mutations detected by NGS in switchover samples failed to expand whenever the patient received the 2GTKI to whom they were insensitive. In contrast, no low level mutation that was resistant to the 2GTKI the patients subsequently received was detected in the switchover samples from Group 2. NGS at the time of imatinib failure reliably identifies clinically relevant mutations, thus enabling a more effective therapeutic tailoring.
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