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

The presence of a BCR-ABL mutant allele in CML does not always explain clinical resistance to imatinib.

Leukemia - 1 Apr 2006

Khorashad J S, Anand M, Marin D, Saunders S, Al-Jabary T, Iqbal A, Margerison S, Melo J V, Goldman J M, Apperley J F, Kaeda J

Abstract excerpt

The expansion of a leukemia clone bearing a Bcr-Abl kinase domain mutation is associated with acquired resistance to imatinib and may also predict disease progression in patients with Philadelphia-positive chronic myeloid leukemia (CML). Here we report results of pyrosequencing to quantitate the non-mutated and mutant alleles in 12 CML patients monitored over periods ranging from 11 to 58 months, and describe...

Read the complete abstract on PubMed

Topics

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

Share to Benzamides
Share to Drug Resistance, Neoplasm

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Fusion Proteins, bcr-abl

Share to Imatinib Mesylate

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

Share to Piperazines

Share to Protein-Tyrosine Kinases

Share to Pyrimidines

Source

Identifiers

PMID: 16467863
DOI: 10.1038/sj.leu.2404137

Genes

BCR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The presence of a BCR-ABL mutant allele in CML does not always explain clinical resistance to imatinib.PMID 16467863Read ↗

Rapid clonal shifts in response to kinase inhibitor therapy in chronic myelogenous leukemia are identified by quantitation mutation assays.Semantic proximity Read ↗

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

Detection of mutations in CML patients resistant to tyrosine kinase inhibitor: imatinib mesylate therapy.Semantic proximity Read ↗

Emerging kinetics of BCR-ABL1 mutations and their effect on disease outcomes in chronic myeloid leukemia patients with imatinib failure.Semantic proximity Read ↗

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

Molecular monitoring in patients with chronic myelogenous leukemia.Semantic proximity Read ↗

Determining the rise in BCR-ABL RNA that optimally predicts a kinase domain mutation in patients with chronic myeloid leukemia on imatinib.Semantic proximity Read ↗

Frequency and clinical significance of BCR-ABL mutations in patients with chronic myeloid leukemia treated with imatinib mesylateSemantic proximity Read ↗

Not all imatinib resistance in CML are BCR-ABL kinase domain mutations.Semantic proximity Read ↗

Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor prognosis.Semantic proximity Read ↗

BCR-ABL kinase domain mutations in chronic myeloid leukemia: not quite enough to cause resistance to imatinib therapy?Semantic proximity Read ↗

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