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

[Origin of resistance to Imatinib mesylate: lessons learned from this experience].

Medecine sciences : M/S - 1 Dec 2004

Roche-Lestienne Catherine, Mahon François-Xavier, Preudhomme Claude

Abstract excerpt

For drug development and pharmaceutical research, targeting the molecular abnormalities is considered as a new challenge. A number of diseases including cancer are linked to perturbation of tyrosine kinase (TK). Imatinib (Glivec or Gleevec, Novartis), the most potent inhibitor of c-abl TK, was recently developed. This molecule has been approved in the treatment of chronic myeloid leukemia (CML). However,...

Read the complete abstract on PubMed

Topics

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

Share to Antineoplastic Agents
Share to Benzamides
Share to Drug Resistance, Neoplasm

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Imatinib Mesylate

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

Share to Piperazines

Share to Protein Kinase Inhibitors

Share to Pyrimidines

Source

Identifiers

PMID: 15581468
DOI: 10.1051/medsci/200420121125

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

[Origin of resistance to Imatinib mesylate: lessons learned from this experience].PMID 15581468Read ↗

Resistance to imatinib: mutations and beyond.Semantic proximity Read ↗

Resistance to tyrosine kinase inhibitors: calling on extra forces.Semantic proximity Read ↗

Clinical resistance to imatinib: mechanisms and implications.Semantic proximity Read ↗

Emerging stem cell concepts for imatinib-resistant chronic myeloid leukaemia: implications for the biology, management, and therapy of the disease.Semantic proximity Read ↗

[Study on the mechanism of imatinib-induced resistance in gastrointestinal stromal tumors].Semantic proximity Read ↗

Mechanisms of resistance to imatinib in CML patients: a paradigm for the advantages and pitfalls of molecularly targeted therapy.Semantic proximity Read ↗

Therapy of Chronic Myeloid Leukemia: Twilight of the Imatinib Era?Semantic proximity Read ↗

Multiple paths to a drug resistance phenotype: mutations, translocations, deletions and amplification of coding genes or promoter regions, epigenetic changes and microRNAs.Semantic proximity Read ↗

Resistance to Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia—From Molecular Mechanisms to Clinical RelevanceSemantic proximity Read ↗

Mechanisms of primary and secondary resistance to imatinib in chronic myeloid leukemia.Semantic proximity Read ↗

Resistance to targeted therapy in chronic myelogenous leukemia.Semantic proximity Read ↗

Resistance to chemotherapy: new treatments and novel insights into an old problemSemantic proximity Read ↗

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