ArticleThe Journal of clinical investigation2012
DYRK1A in Down syndrome: an oncogene or tumor suppressor?
Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- The very rare association between T-cell acute lymphoblastic leukemia and down syndrome: a case report and review of the literature.Frontiers in pediatrics · 2026Article
- Diabetic Kinome Inhibitors-A New Opportunity for β-Cells Restoration.International journal of molecular sciences · 2021Review
- Dual-Specificity, Tyrosine Phosphorylation-Regulated Kinases (DYRKs) and cdc2-Like Kinases (CLKs) in Human Disease, an Overview.International journal of molecular sciences · 2021Review
- Ten Reasons Why People With Down Syndrome are Protected From the Development of Most Solid Tumors -A Review.Frontiers in genetics · 2021Review
- The nuclear interactome of DYRK1A reveals a functional role in DNA damage repair.Scientific reports · 2019Article
- Low risk of solid tumors in persons with Down syndrome.Genetics in medicine : official journal of the American College of Medical Genetics · 2016Article
- Tumor suppressor DYRK1A effects on proliferation and chemoresistance of AML cells by downregulating c-Myc.PloS one · 2014Article
- Tumorigenesis in Down's syndrome: big lessons from a small chromosome.Nature reviews. Cancer · 2012Article
- DYRK1A: the double-edged kinase as a protagonist in cell growth and tumorigenesis.Molecular & cellular oncologyReview
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Children with Down syndrome (DS) have a markedly increased risk of developing acute megakaryoblastic leukemia (AMKL) and acute lymphoblastic leukemia compared with that of children without DS. Despite recent breakthroughs, it is not clear which genes on chromosome 21, the chromosome that is trisomic in individuals with DS, cause this predisposition. In this issue of the JCI, Malinge et al. report their loss- and gain-of-function experiments in mouse and human cells that show that increased expression of the kinase encoded by the chromosome 21 gene DYRK1A suppresses the nuclear factor of activated T cells pathway and promotes AMKL. Interestingly, the same protein has been suggested to contribute to the reduced risk of epithelial cancers in adults with DS, leading to the possibility that it could be proleukemic in children and antitumorigenic in adults.
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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.