ArticleBlood2011
Oncogenic tyrosine kinase NPM-ALK induces expression of the growth-promoting receptor ICOS.
Article in Blood, 2011. 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, 37 citations in OpenAlex.
- HDAC1 acts as a tumor suppressor in ALK-positive anaplastic large cell lymphoma: implications for HDAC inhibitor therapy.Leukemia · 2025Article
- Chimeric kinase ALK induces expression of NAMPT and selectively depends on this metabolic enzyme to sustain its own oncogenic function.Leukemia · 2023Article
- Updates in pathobiological aspects of anaplastic large cell lymphoma.Frontiers in oncology · 2023Review
- Induction of Transcriptional Inhibitor HES1 and the Related Repression of Tumor-Suppressor TXNIP Are Important Components of Cell-Transformation Program Imposed by Oncogenic Kinase NPM-ALK.The American journal of pathology · 2022Article
- Colony-Stimulating Factor 1 Receptor (CSF1R) Activates AKT/mTOR Signaling and Promotes T-Cell Lymphoma Viability.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- Systems and Synthetic microRNA Biology: From Biogenesis to Disease Pathogenesis.International journal of molecular sciences · 2019Review
- Crosstalk between microRNA and DNA Methylation Offers Potential Biomarkers and Targeted Therapies in ALK-Positive Lymphomas.Cancers · 2017Review
- Genetics of anaplastic large cell lymphoma.Leukemia & lymphoma · 2016Article
- A three-signal model of T-cell lymphoma pathogenesis.American journal of hematology · 2016Review
- [The research progress of costimulatory molecule B7 family in hematological malignancy].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2015Article
- Cutaneous T cell lymphoma expresses immunosuppressive CD80 (B7-1) cell surface protein in a STAT5-dependent manner.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Dysregulation of microRNAs and their association in the pathogenesis of T-cell lymphoma/leukemias.International journal of hematology · 2014Review
- Beyond NPM-anaplastic lymphoma kinase driven lymphomagenesis: alternative drivers in anaplastic large cell lymphoma.Current opinion in hematology · 2013Review
- The pathobiology of the oncogenic tyrosine kinase NPM-ALK: a brief update.Therapeutic advances in hematology · 2013Article
- Review
- STAT3 signaling induces the differentiation of human ICOS(+) CD4 T cells helping B lymphocytes.PloS one · 2013Article
- miR-219-5p inhibits receptor tyrosine kinase pathway by targeting EGFR in glioblastoma.PloS one · 2013Article
- New molecular insights into peripheral T cell lymphomas.The Journal of clinical investigation · 2012Review
- Article
- NPM-ALK: The Prototypic Member of a Family of Oncogenic Fusion Tyrosine Kinases.Journal of signal transduction · 2012Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
Here we report that T-cell lymphoma cells carrying the NPM-ALK fusion protein (ALK(+) TCL) frequently express the cell-stimulatory receptor ICOS. ICOS expression in ALK(+) TCL is moderate and strictly dependent on the expression and enzymatic activity of NPM-ALK. NPM-ALK induces ICOS expression via STAT3, which triggers the transcriptional activity of the ICOS gene promoter. In addition, STAT3 suppresses the expression of miR-219 that, in turn, selectively inhibits ICOS expression. ALK(+) TCL cell lines display extensive DNA methylation of the CpG island located within intron 1, the putative enhancer region, of the ICOS gene, whereas cutaneous T-cell lymphoma cell lines, which strongly express ICOS, show no methylation of the island. Treatment of the ALK(+) TCL cell lines with DNA methyltransferase inhibitor reversed the CpG island methylation and augmented the expression of ICOS mRNA and protein. Stimulation of the ICOS receptor with anti-ICOS antibody or ICOS ligand-expressing B cells markedly enhanced proliferation of the ALK(+) TCL cells. These results demonstrate that NPM-ALK, acting through STAT3 as the gene transcriptional activator, induces the expression of ICOS, a cell growth promoting receptor. These data also show that the DNA methylation status of the intronic CpG island affects transcriptional activity of the ICOS gene and, consequently, modulates the concentration of the expressed ICOS protein.
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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.