ArticleBlood cancer journal2011
Gene expression signatures associated with the in vitro resistance to two tyrosine kinase inhibitors, nilotinib and imatinib.
Article in Blood cancer journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Emerging Roles of YES1 in Cancer: The Putative Target in Drug Resistance.International journal of molecular sciences · 2024Review
- Therapies for Tau-associated neurodegenerative disorders: targeting molecules, synapses, and cells.Neural regeneration research · 2023Article
- Role of YES1 signaling in tumor therapy resistance.Cancer innovation · 2023Review
- Molecular Mechanisms of Tyrosine Kinase Inhibitor Resistance in Chronic Myeloid Leukemia.Handbook of experimental pharmacology · 2023Review
- Profiling the Expression and Prognostic Values of FYN, A Non-Receptor Tyrosine Kinase, in Different Histological Types of Epithelial Ovarian Cancer.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Genome‑wide expression and methylation analyses reveal aberrant cell adhesion signaling in tyrosine kinase inhibitor‑resistant CML cells.Oncology reports · 2022Article
- Systematic prediction of drug resistance caused by transporter genes in cancer cells.Scientific reports · 2021Article
- Review
- GCA links TRAF6-ULK1-dependent autophagy activation in resistant chronic myeloid leukemia.Autophagy · 2019Article
- Imatinib-Induced Changes in Protein Expression and ATP-Binding Affinities of Kinases in Chronic Myelocytic Leukemia Cells.Analytical chemistry · 2019Article
- Long noncoding RNA DANCR contributes to docetaxel resistance in prostate cancer through targeting the miR-34a-5p/JAG1 pathway.OncoTargets and therapy · 2019Article
- Cobll1 is linked to drug resistance and blastic transformation in chronic myeloid leukemia.Leukemia · 2017Article
- Article
- Network pharmacology strategies toward multi-target anticancer therapies: from computational models to experimental design principles.Current pharmaceutical design · 2014Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The use of selective inhibitors targeting Bcr-Abl kinase is now established as a standard protocol in the treatment of chronic myelogenous leukemia; however, the acquisition of drug resistance is a major obstacle limiting the treatment efficacy. To elucidate the molecular mechanism of drug resistance, we established K562 cell line models resistant to nilotinib and imatinib. Microarray-based transcriptome profiling of resistant cells revealed that nilotinib- and imatinib-resistant cells showed the upregulation of kinase-encoding genes (AURKC, FYN, SYK, BTK and YES1). Among them, the upregulation of AURKC and FYN was observed both in nilotinib- and imatinib-resistant cells irrespective of exposure doses, while SYK, BTK and YES1 showed dose-dependent upregulation of expression. Upregulation of EGF and JAG1 oncogenes as well as genes encoding ATP-dependent drug efflux pump proteins such as ABCB1 was also observed in the resistant cells, which may confer alternative survival benefits. Functional gene set analysis revealed that molecular categories of 'ATPase activity', 'cell adhesion' or 'tyrosine kinase activity' were commonly activated in the resistant clones. Taken together, the transcriptome analysis of tyrosine kinase inhibitors (TKI)-resistant clones provides the insights into the mechanism of drug resistance, which can facilitate the development of an effective screening method as well as therapeutic intervention to deal with TKI resistance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.