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

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

Blood - 24 Sept 2009

Press Richard D, Willis Stephanie G, Laudadio Jennifer, Mauro Michael J, Deininger Michael W N

Abstract excerpt

In imatinib-treated chronic myeloid leukemia (CML), secondary drug resistance is often caused by mutations in the BCR-ABL kinase domain (KD). As alternative therapies are available for imatinib resistance, early identification of mutations may prevent disease progression. Because most patients are routinely monitored by BCR-ABL quantitative polymerase chain reaction (PCR), it is important to define the optimal...

Read the complete abstract on PubMed

Topics

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

Share to Benzamides
Share to Fusion Proteins, bcr-abl

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Expression Regulation, Leukemic

Share to Imatinib Mesylate

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

Share to Phosphotransferases

Share to Piperazines

Share to Pyrimidines

Source

Open in PubMed Open full text

Identifiers

PMID: 19625707
DOI: 10.1182/blood-2008-08-173674
PMCID: PMC2756120

Genes

BCR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Determining the rise in BCR-ABL RNA that optimally predicts a kinase domain mutation in patients with chronic myeloid leukemia on imatinib.PMID 19625707Read ↗

Real-time quantitative PCR analysis can be used as a primary screen to identify patients with CML treated with imatinib who have BCR-ABL kinase domain mutationsSemantic proximity Read ↗

The role of serial BCR-ABL transcript monitoring in predicting the emergence of BCR-ABL kinase mutations in imatinib-treated patients with chronic myeloid leukemia.Semantic proximity Read ↗

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

Constant BCR-ABL transcript level >or=0.1% (IS) in patients with CML responding to imatinib with complete cytogenetic remission may indicate mutation analysis.Semantic proximity Read ↗

Molecular monitoring in patients with chronic myelogenous leukemia.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 ↗

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

BCR-ABL messenger RNA levels continue to decline in patients with chronic phase chronic myeloid leukemia treated with imatinib for more than 5 years and approximately half of all first-line treated patients have stable undetectable BCR-ABL using strict sensitivity criteria.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 ↗

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

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

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