ArticleOncotarget2014
The ALK inhibitor ASP3026 eradicates NPM-ALK⁺ T-cell anaplastic large-cell lymphoma in vitro and in a systemic xenograft lymphoma model.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- DAB2IP suppresses invadopodia formation through destabilizing ALK by interacting with USP10 in breast cancer.iScience · 2023Article
- Preclinical Evaluation of Gilteritinib on NPM1-ALK-Driven Anaplastic Large Cell Lymphoma Cells.Molecular cancer research : MCR · 2021Article
- Activation of IGF-1R pathway and NPM-ALK G1269A mutation confer resistance to crizotinib treatment in NPM-ALK positive lymphoma.Investigational new drugs · 2020Article
- Recombinant expression, characterization, and quantification in human cancer cell lines of the Anaplastic Large-Cell Lymphoma-characteristic NPM-ALK fusion protein.Scientific reports · 2020Article
- ALK and RET Inhibitors Promote HLA Class I Antigen Presentation and Unmask New Antigens within the Tumor Immunopeptidome.Cancer immunology research · 2019Article
- Dual inhibition of IGF-IR and ALK as an effective strategy to eradicate NPM-ALKJournal of hematology & oncology · 2019Article
- Development and Significance of Mouse Models in Lymphoma Research.Current hematologic malignancy reports · 2019Review
- Anaplastic lymphoma kinase fusions: Roles in cancer and therapeutic perspectives.Oncology letters · 2019Review
- Characterization and diagnostic application of genomicOncotarget · 2018Article
- Review
- TrkA is a binding partner of NPM-ALK that promotes the survival of ALKMolecular oncology · 2017Article
- The long non-coding RNA LINC01013 enhances invasion of human anaplastic large-cell lymphoma.Scientific reports · 2017Article
- ALK: a tyrosine kinase target for cancer therapy.Cold Spring Harbor molecular case studies · 2017Review
- LncRNA MALAT1 promotes development of mantle cell lymphoma by associating with EZH2.Journal of translational medicine · 2016Article
- TKI sensitivity patterns of novel kinase-domain mutations suggest therapeutic opportunities for patients with resistant ALK+ tumors.Oncotarget · 2016Article
- Validation of a Preclinical Model of Diethylnitrosamine-Induced Hepatic Neoplasia in Yucatan Miniature Pigs.Oncology · 2016Article
- Targeting autophagy enhances the anti-tumoral action of crizotinib in ALK-positive anaplastic large cell lymphoma.Oncotarget · 2015Article
- SUMOylation Confers Posttranslational Stability on NPM-ALK Oncogenic Protein.Neoplasia (New York, N.Y.) · 2015Article
- Targeting Notch1 and proteasome as an effective strategy to suppress T-cell lymphoproliferative neoplasms.Oncotarget · 2015Article
- NPM/ALK mutants resistant to ASP3026 display variable sensitivity to alternative ALK inhibitors but succumb to the novel compound PF-06463922.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
NPM-ALK⁺ T-cell anaplastic large-cell lymphoma (ALCL) is an aggressive type of cancer. Standard treatment of NPM-ALK⁺ ALCL is CHOP polychemotherapy. Although patients initially respond favorably to CHOP, resistance, relapse, and death frequently occur. Recently, selective targeting of ALK has emerged as an alternative therapeutic strategy. ASP3026 is a second-generation ALK inhibitor that can overcome crizotinib resistance in non-small cell lung cancer, and is currently being evaluated in clinical trials of patients with ALK⁺ solid tumors. However, NPM-ALK⁺ ALCL patients are not included in these trials. We studied the effects of ASP3026 on NPM-ALK⁺ ALCL cell lines in vitro and on systemic lymphoma growth in vivo. ASP3026 decreased the viability, proliferation, and colony formation, as well as induced apoptotic cell death of NPM-ALK⁺ ALCL cells. In addition, ASP3026 significantly reduced the proliferation of 293T cells transfected with NPM-ALK mutants that are resistant to crizotinib and downregulated tyrosine phosphorylation of these mutants. Moreover, ASP3026 abrogated systemic NPM-ALK⁺ ALCL growth in mice. Importantly, the survival of ASP3026-treated mice was superior to that of control and CHOP-treated mice. Our data suggest that ASP3026 is an effective treatment for NPM-ALK⁺ ALCL, and support the enrollment of patients with this lymphoma in the ongoing clinical trials.
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