ArticleBlood2009
IGF-IR tyrosine kinase interacts with NPM-ALK oncogene to induce survival of T-cell ALK+ anaplastic large-cell lymphoma cells.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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Who cites it
31 citing papers in PubMed, 59 citations in OpenAlex.
- Three decades of anaplastic lymphoma kinase: from physiological roles to cancer and immune evasion.Cancer metastasis reviews · 2026Review
- ALK fusions in the pan-cancer setting: another tumor-agnostic target?NPJ precision oncology · 2023Review
- Tyrosine phosphatases regulate resistance to ALK inhibitors in ALK+ anaplastic large cell lymphoma.Blood · 2022Article
- Holistic View of ALK TKI Resistance in ALK-Positive Anaplastic Large Cell Lymphoma.Frontiers in oncology · 2022Review
- Review
- Chemerin reverses the malignant phenotype and induces differentiation of human hepatoma SMMC7721 cells.Archives of pharmacal research · 2021Article
- Insulin-like growth factor receptor signaling in tumorigenesis and drug resistance: a challenge for cancer therapy.Journal of hematology & oncology · 2020Review
- Activation of IGF-1R pathway and NPM-ALK G1269A mutation confer resistance to crizotinib treatment in NPM-ALK positive lymphoma.Investigational new drugs · 2020Article
- Review
- Dual inhibition of IGF-IR and ALK as an effective strategy to eradicate NPM-ALKJournal of hematology & oncology · 2019Article
- TrkA is a binding partner of NPM-ALK that promotes the survival of ALKMolecular oncology · 2017Article
- Type I insulin-like growth factor receptor signaling in hematological malignancies.Oncotarget · 2017Review
- Endogenous dendritic cells from the tumor microenvironment support T-ALL growth via IGF1R activation.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Crizotinib-induced antitumour activity in human alveolar rhabdomyosarcoma cells is not solely dependent on ALK and MET inhibition.Journal of experimental & clinical cancer research : CR · 2015Article
- SUMOylation Confers Posttranslational Stability on NPM-ALK Oncogenic Protein.Neoplasia (New York, N.Y.) · 2015Article
- Picropodophyllin inhibits proliferation and survival of diffuse large B-cell lymphoma cells.Medical oncology (Northwood, London, England) · 2015Article
- Targeting Notch1 and proteasome as an effective strategy to suppress T-cell lymphoproliferative neoplasms.Oncotarget · 2015Article
- Therapeutic targeting of anaplastic lymphoma kinase in lung cancer: a paradigm for precision cancer medicine.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Review
- The transcription factors Ik-1 and MZF1 downregulate IGF-IR expression in NPM-ALK⁺ T-cell lymphoma.Molecular cancer · 2015Article
- Cytotoxic effects of loperamide hydrochloride on canine cancer cells.The Journal of veterinary medical science · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Type I insulin-like growth factor receptor (IGF-IR) tyrosine kinase plays important roles in the pathogenesis of several malignancies. Although it promotes the growth of stimulated hematopoietic cells, a direct role of IGF-IR in malignant lymphoma has not been identified. Anaplastic lymphoma kinase-positive anaplastic large-cell lymphoma (ALK(+) ALCL) is a unique type of T-cell lymphoma. Approximately 85% of ALK(+) ALCL cases harbor the translocation t(2;5)(p23;q35), which generates the chimeric oncogene NPM-ALK. In the present study, we explored a possible role of IGF-IR in ALK(+) ALCL. Our results demonstrate that IGF-IR and IGF-I are widely expressed in ALK(+) ALCL cell lines and primary tumors. Importantly, we identified novel reciprocal functional interactions between IGF-IR and NPM-ALK. Antagonism of IGF-IR decreased the viability, induced apoptosis and cell-cycle arrest, and decreased proliferation and colony formation of ALK(+) ALCL cell lines. These effects could be explained by alterations of cell survival regulatory proteins downstream of IGF-IR signaling. Our findings improve current understanding of the biology of IGF-IR and NPM-ALK and have significant therapeutic implications as they identify IGF-IR signaling as a potential therapeutic target in ALK(+) ALCL and possibly other types of malignant lymphoma.
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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.