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Article

Proteomic analysis of imatinib-resistant CML-T1 cells reveals calcium homeostasis as a potential therapeutic target.

Oncology reports - 1 Sept 2016

Toman O, Kabickova T, Vit O, Fiser R, Polakova K Machova, Zach J, Linhartova J, Vyoral D, Petrak J

Abstract excerpt

Chronic myeloid leukemia (CML) therapy has markedly improved patient prognosis after introduction of imatinib mesylate for clinical use. However, a subset of patients develops resistance to imatinib and other tyrosine kinase inhibitors (TKIs), mainly due to point mutations in the region encoding the kinase domain of the fused BCR-ABL oncogene. To identify potential therapeutic targets in imatinib‑resistant CML...

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Share to Calcium
Share to Drug Resistance, Neoplasm

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Fusion Proteins, bcr-abl

Share to Homeostasis

Share to Imatinib Mesylate

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

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Source

Open in PubMed Open full text

Identifiers

PMID: 27430982
DOI: 10.3892/or.2016.4945
PMCID: PMC4968618

Genes

BCR
NHERF1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

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