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

BCR-ABL alternative splicing as a common mechanism for imatinib resistance: evidence from molecular dynamics simulations.

Molecular cancer therapeutics - 1 Dec 2008

Lee Tai-Sung, Ma Wanlong, Zhang Xi, Giles Francis, Cortes Jorge, Kantarjian Hagop, Albitar Maher

Abstract excerpt

Rare cases of chronic myelogenous leukemia (CML) express high levels of alternatively spliced BCR-ABL mRNA with a 35-bp insertion (35INS) between ABL kinase domain exons 8 and 9. This insertion results in a frameshift leading to the addition of 10 residues and truncation of 653 residues due to early termination. Sensitive PCR-based testing showed that 32 of 52 (62%) imatinib-resistant CML patients in chronic...

Read the complete abstract on PubMed

Topics

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

Share to Alternative Splicing
Share to Benzamides

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Fusion Proteins, bcr-abl

Share to Imatinib Mesylate

Share to Molecular Conformation

Share to Piperazines

Share to Proto-Oncogene Proteins c-abl

Share to Pyrimidines

Source

Identifiers

PMID: 19056677
DOI: 10.1158/1535-7163.MCT-08-0482

Genes

BCR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

BCR-ABL alternative splicing as a common mechanism for imatinib resistance: evidence from molecular dynamics simulations.PMID 19056677Read ↗

Three novel alternative splicing mutations in BCR-ABL1 detected in CML patients with resistance to kinase inhibitors.Semantic proximity Read ↗

Basis for resistance to imatinib in 16 BCR-ABL mutants as determined using molecular dynamics.Semantic proximity Read ↗

T315I-mutated Bcr-Abl in chronic myeloid leukemia and imatinib: insights from a computational studySemantic proximity Read ↗

Genetic alterations in the BCR-ABL1 fusion gene related to imatinib resistance in chronic myeloid leukemia.Semantic proximity Read ↗

Resistance to imatinib in patients with chronic myelogenous leukemia and the splice variant BCR-ABL1 35INSSemantic proximity Read ↗

Mutation in Abl kinase with altered drug binding kinetics indicates a novel mechanism of imatinib resistanceSemantic proximity Read ↗

Overriding imatinib resistance with a novel ABL kinase inhibitor.Semantic proximity Read ↗

Structural biology contributions to the discovery of drugs to treat chronic myelogenous leukaemiaSemantic proximity Read ↗

Mutation in Abl kinase with altered drug-binding kinetics indicates a novel mechanism of imatinib resistance.Semantic proximity Read ↗

Regulatory SH3-SH2 domain mutations in BCR–ABL1 drive imatinib resistance and confer dasatinib sensitivity in chronic myeloid leukemiaSemantic proximity Read ↗

Tyrosine kinase inhibitors induce alternative spliced BCR-ABLIns35bp variant via inhibition of RNA polymerase II on genomic BCR-ABL.Semantic proximity Read ↗

Structural modeling of V299L and E459K Bcr-Abl mutation, and sequential therapy of tyrosine kinase inhibitors for the compound mutations.Semantic proximity Read ↗

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