ArticleOncogene2003
Vav-promoter regulated oncogenic fusion protein NPM-ALK in transgenic mice causes B-cell lymphomas with hyperactive Jun kinase.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 66 citations in OpenAlex.
- Comprehensive genomic analysis reveals molecular heterogeneity in pediatric ALK-positive anaplastic large cell lymphoma.Research square · 2024Article
- Junction of the redox dynamic, orchestra of signaling, and altered metabolism in regulation of T- cell lymphoma.Frontiers in oncology · 2023Review
- De novo generation of the NPM-ALK fusion recapitulates the pleiotropic phenotypes of ALK+ ALCL pathogenesis and reveals the ROR2 receptor as target for tumor cells.Molecular cancer · 2022Article
- BRG1 and NPM-ALK Are Co-Regulated in Anaplastic Large-Cell Lymphoma; BRG1 Is a Potential Therapeutic Target in ALCL.Cancers · 2021Article
- Review
- Article
- CRISPR genome editing of murine hematopoietic stem cells to createBlood advances · 2019Article
- Article
- Insights into the Pathogenesis of Anaplastic Large-Cell Lymphoma through Genome-wide DNA Methylation Profiling.Cell reports · 2016Article
- Challenging perspectives on the cellular origins of lymphoma.Open biology · 2016Article
- Anaplastic large cell lymphoma arises in thymocytes and requires transient TCR expression for thymic egress.Nature communications · 2016Article
- Molecular Pathogenesis of Peripheral T Cell Lymphoma.Current hematologic malignancy reports · 2015Review
- Oncogenic role of miR-155 in anaplastic large cell lymphoma lacking the t(2;5) translocation.The Journal of pathology · 2015Article
- Article
- Human Vav1 expression in hematopoietic and cancer cell lines is regulated by c-Myb and by CpG methylation.PloS one · 2012Article
- Determining the contribution of NPM1 heterozygosity to NPM-ALK-induced lymphomagenesis.Laboratory investigation; a journal of technical methods and pathology · 2011Article
- Article
- Oncogenic mutations of ALK in neuroblastoma.Cancer science · 2011Review
- Identification of differential and functionally active miRNAs in both anaplastic lymphoma kinase (ALK)+ and ALK- anaplastic large-cell lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Molecular pathogenesis of peripheral neuroblastic tumors.Oncogene · 2010Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anaplastic large-cell lymphoma is associated with a chromosomal translocation generating an oncogenic fusion protein: the nucleophosmin-anaplastic lymphoma kinase (NPM-ALK). We have generated several independent lines of human NPM-ALK transgenic mice using the haematopoietic cell-specific Vav promoter. Lymphomas develop in two transgenic lines in which the Vav promoter regulates NPM-ALK expression. The transgenic line with higher copy number displays an early-onset phenotype in which all mice succumb to aggressive lymph node tumours with intestinal involvement, whereas the second line displays late-onset tumour development in the spleen and/or liver. Lymphomas from both lines are phenotypically distinct and display B-lineage characteristics with aberrant coexpression of myeloid markers. The NPM-ALK kinase is active in primary tumour tissue and forms a multimeric complex with tyrosine-phosphorylated proteins, that is, Shc. Jun and ERK kinase activities in tumours are elevated by up to 30-fold and fivefold, respectively, in comparison with sIgM-stimulated primary B cells. The new transgenic models provide a system for investigating the oncogenic events mediated by NPM-ALK in situ and a physiologically relevant context for developing tyrosine kinase inhibitor therapies of potential use in the clinic.
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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.