Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Detection of drug-resistant clones in chronic myelogenous leukemia patients during dasatinib and nilotinib treatment.

Clinical chemistry - 1 Mar 2010

Gruber Franz X, Ernst Thomas, Kiselev Yuri, Hochhaus Andreas, Mikkola Ingvild

Abstract excerpt

BACKGROUND: Imatinib effectively inhibits the tyrosine kinase activity conferred by the BCR-ABL gene [fusion gene of BCR (breakpoint cluster region) and ABL1 (c-abl oncogene 1, receptor tyrosine kinase)] and thereby appreciably improves outcomes for chronic myelogenous leukemia (CML). A small percentage of patients relapse because of the proliferation of escape clones; such relapses can be treated with...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Clone Cells
Share to Dasatinib
Share to Drug Resistance, Neoplasm

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Fusion Proteins, bcr-abl

Share to Leukemia, Myelogenous, Chronic, BCR-ABL Positive

Share to Protein Kinase Inhibitors

Share to Pyrimidines

Share to Thiazoles

Source

Identifiers

PMID: 20040619
DOI: 10.1373/clinchem.2009.133843

Genes

BCR
ABL1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Detection of drug-resistant clones in chronic myelogenous leukemia patients during dasatinib and nilotinib treatment.PMID 20040619Read ↗

Sensitive detection of BCR-ABL1 mutations in patients with chronic myeloid leukemia after imatinib resistance is predictive of outcome during subsequent therapy.Semantic proximity Read ↗

Detection of BCR-ABL mutations and resistance to imatinib mesylate.Semantic proximity Read ↗

A co-operative evaluation of different methods of detecting BCR-ABL kinase domain mutations in patients with chronic myeloid leukemia on second-line dasatinib or nilotinib therapy after failure of imatinib.Semantic proximity Read ↗

Detection of BCR-ABL1 kinase domain mutations causing imatinib resistance in chronic myelogenous leukemia.Semantic proximity Read ↗

Denaturing-HPLC-Based Assay for Detection of ABL Mutations in Chronic Myeloid Leukemia Patients Resistant to ImatinibSemantic proximity Read ↗

Monitoring minimal residual disease and controlling drug resistance in chronic myeloid leukaemia patients in treatment with imatinib as a guide to clinical management.Semantic proximity Read ↗

BCR-ABL1 kinase domain mutations: methodology and clinical evaluation.Semantic proximity Read ↗

In chronic myeloid leukemia patients on second-line tyrosine kinase inhibitor therapy, deep sequencing of BCR-ABL1 at the time of warning may allow sensitive detection of emerging drug-resistant mutants.Semantic proximity Read ↗

Poor response to second-line kinase inhibitors in chronic myeloid leukemia patients with multiple low-level mutations, irrespective of their resistance profile.Semantic proximity Read ↗

BCR-ABL1 RT-qPCR for monitoring the molecular response to tyrosine kinase inhibitors in chronic myeloid leukemia.Semantic proximity Read ↗

Frequency of ABL gene mutations in chronic myeloid leukemia patients resistant to imatinib and results of treatment switch to second-generation tyrosine kinase inhibitors.Semantic proximity Read ↗

High-sensitivity detection of BCR-ABL kinase domain mutations in imatinib-naive patients: correlation with clonal cytogenetic evolution but not response to therapy.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.