ArticleOncotarget2011
Mechanisms of AXL overexpression and function in Imatinib-resistant chronic myeloid leukemia cells.
Article in Oncotarget, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 118 citations in OpenAlex.
- Window-of-Opportunity Study Utilizing Preoperative Cetuximab in Patients with Head and Neck Cancer.Cancer research communications · 2026Article
- Discovery of potential AXL inhibitors using virtual screening, molecular docking, molecular dynamics, molecular mechanics, and in vitro validation.Scientific reports · 2026Article
- LIN28A-Dependent Kinome and Phosphoproteome Reprogramming Promotes Imatinib Resistance.Molecular & cellular proteomics : MCP · 2026Article
- Kaempferols from Echinacea purpurea demonstrate anti-cancer potential by targeting anexelekto in breast cancer therapy using chemoinformatics approach.Discover oncology · 2025Article
- TAM family kinases are potential candidate targets for therapeutic intervention in chronic myeloid leukemia.Discover oncology · 2025Article
- Paratope mapping of tilvestamab, an anti-AXL function-blocking antibody, using high-throughput bacterial expression of secreted scFv-osmY fusion proteins.Bioscience reports · 2025Article
- Genetic Profiling of Acute and Chronic Leukemia via Next-Generation Sequencing: Current Insights and Future Perspectives.Hematology reports · 2025Review
- AXL: shapers of tumor progression and immunosuppressive microenvironments.Molecular cancer · 2025Review
- Combination Therapy With Asciminib and Ponatinib as a Bridge to Brexucabtagene Autoleucel and Maintenance in a Patient With Relapsed Refractory Philadelphia Positive B-Cell Acute Lymphoblastic Leukemia.Journal of medical cases · 2024Article
- Article
- TAM family kinases as therapeutic targets at the interface of cancer and immunity.Nature reviews. Clinical oncology · 2023Review
- AXL/Gas6 signaling mechanisms in the hypothalamic-pituitary-gonadal axis.Frontiers in endocrinology · 2023Review
- Preclinical Development of ADCT-601, a Novel Pyrrolobenzodiazepine Dimer-based Antibody-drug Conjugate Targeting AXL-expressing Cancers.Molecular cancer therapeutics · 2022Article
- Dissecting the Role of AXL in Cancer Immune Escape and Resistance to Immune Checkpoint Inhibition.Frontiers in immunology · 2022Review
- Therapeutic Targeting of the Gas6/Axl Signaling Pathway in Cancer.International journal of molecular sciences · 2021Review
- Multiple malignant tumors in a patient with familial chordoma, a case report.BMC medical genomics · 2021Article
- Non-Coding RNAs Set a New Phenotypic Frontier in Prostate Cancer Metastasis and Resistance.International journal of molecular sciences · 2021Review
- Plk1, upregulated by HIF-2, mediates metastasis and drug resistance of clear cell renal cell carcinoma.Communications biology · 2021Article
- Efficacy of newly discovered DNA aptamers targeting AXL in a lung cancer cell with acquired resistance to Erlotinib.Translational cancer research · 2021Article
- AXL Mediates Cetuximab and Radiation Resistance Through Tyrosine 821 and the c-ABL Kinase Pathway in Head and Neck Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AXL is a receptor tyrosine kinase of the TAM family, the function of which is poorly understood. We previously identified AXL overexpression in Imatinib (IM)-resistant CML cell lines and patients. The present study was conducted to investigate the role of AXL and the mechanisms underlying AXL overexpression in Tyrosine Kinase Inhibitor (TKI)-resistant CML cells. We present evidence that high AXL expression level is a feature of TKI-resistant CML cells and knockdown of AXL sensitized TKI-resistant cells to IM. In addition, expression of wild-type AXL but not a dominant negative form of AXL confers IM-sensitive CML cells the capacity to resist IM effect. AXL overexpression required PKCα and β and constitutive activation of ERK1/2. Accordingly, GF109203X a PKC inhibitor, U0126 a MEK1 inhibitor and PKCα/β knockdown restore sensitivity to IM while PKCα or PKCβ overexpression in CML cells promotes protection against IM-induced cell death. Finally, using luciferase promoter activity assays we established that AXL is regulated transcriptionally through the AP1 transcription factor. Our findings reveal an unexpected role of AXL in resistance to TKI in CML cells, identify the molecular mechanisms involved in its overexpression and support the notion that AXL is a new marker of resistance to TKI in CML.
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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.