ArticleJournal of signal transduction2012
NPM-ALK: The Prototypic Member of a Family of Oncogenic Fusion Tyrosine Kinases.
Article in Journal of signal transduction, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
- Cancer-associated fusion transcripts: mechanisms, functional roles, and clinical implications.Clinical and experimental medicine · 2026Review
- Regulation of PD-L1 Expression by SAHA-Mediated Histone Deacetylase Inhibition in Lung Cancer Cells.Cancers · 2025Article
- Circulating tumor DNA in ALK-positive anaplastic large cell lymphoma: a proof-of-concept study.NPJ precision oncology · 2025Article
- Review
- Article
- Unraveling the Potential of ALK-Targeted Therapies in Non-Small Cell Lung Cancer: Comprehensive Insights and Future Directions.Biomedicines · 2024Review
- TCR Pathway Mutations in Mature T Cell Lymphomas.Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- PD-1/PD-L1 Pathway: A Therapeutic Target in CD30+ Large Cell Lymphomas.Biomedicines · 2022Review
- Review
- Identification of Hub Genes and Key Pathways Associated with Peripheral T-cell Lymphoma.Current medical science · 2020Article
- Diagnostic Capability of Next-Generation Sequencing Fusion Analysis in Identifying a Rare CASE ofFrontiers in oncology · 2020Article
- Data driven polypharmacological drug design for lung cancer: analyses for targeting ALK, MET, and EGFR.Journal of cheminformatics · 2017Article
- Pediatric, Adolescent, and Young Adult Thyroid Carcinoma Harbors Frequent and Diverse Targetable Genomic Alterations, Including Kinase Fusions.The oncologist · 2017Article
- Anaplastic large cell lymphoma: pathology, genetics, and clinical aspects.Journal of clinical and experimental hematopathology : JCEH · 2017Review
- TKI sensitivity patterns of novel kinase-domain mutations suggest therapeutic opportunities for patients with resistant ALK+ tumors.Oncotarget · 2016Article
- Fusion genes with ALK as recurrent partner in ependymoma-like gliomas: a new brain tumor entity?Neuro-oncology · 2015Article
- Article
- Detection of a TRAF1-ALK fusion in an anaplastic large cell lymphoma patient with chemotherapy and ALK inhibitor-resistant disease.BMC research notes · 2015Article
- Evidence Suggesting That Discontinuous Dosing of ALK Kinase Inhibitors May Prolong Control of ALK+ Tumors.Cancer research · 2015Article
- NPM-ALK mediates phosphorylation of MSH2 at tyrosine 238, creating a functional deficiency in MSH2 and the loss of mismatch repair.Blood cancer journal · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anaplastic lymphoma kinase (ALK) was first identified in 1994 with the discovery that the gene encoding for this kinase was involved in the t(2;5)(p23;q35) chromosomal translocation observed in a subset of anaplastic large cell lymphoma (ALCL). The NPM-ALK fusion protein generated by this translocation is a constitutively active tyrosine kinase, and much research has focused on characterizing the signalling pathways and cellular activities this oncoprotein regulates in ALCL. We now know about the existence of nearly 20 distinct ALK translocation partners, and the fusion proteins resulting from these translocations play a critical role in the pathogenesis of a variety of cancers including subsets of large B-cell lymphomas, nonsmall cell lung carcinomas, and inflammatory myofibroblastic tumours. Moreover, the inhibition of ALK has been shown to be an effective treatment strategy in some of these malignancies. In this paper we will highlight malignancies where ALK translocations have been identified and discuss why ALK fusion proteins are constitutively active tyrosine kinases. Finally, using ALCL as an example, we will examine three key signalling pathways activated by NPM-ALK that contribute to proliferation and survival in ALCL.
Identifiers
What OpenQuestion holds
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.