ArticleBlood2020
CDK6 is an essential direct target of NUP98 fusion proteins in acute myeloid leukemia.
Article in Blood, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 76 citations in OpenAlex.
- Uncovering essential RNA components of fusion oncoprotein condensates using bicon-seq.The EMBO journal · 2026Article
- Advances in targeted therapies for pediatric tumors.Acta pharmacologica Sinica · 2026Article
- Cell-cycle targeted cancer therapy: clinical advances, biological gaps, and the emergence of selective CDK4 inhibitors.Journal of hematology & oncology · 2026Review
- Combined Menin and XPO1 inhibition drive synergistic antileukemic activity inbioRxiv : the preprint server for biology · 2026Article
- Phase-separating fusion proteins drive cancer by upsetting transcription regulation.Genome biology · 2025Article
- Image-based drug screening combined with molecular profiling identifies signatures and drivers of therapy resistance in pediatric AML.Cell reports. Medicine · 2025Article
- Clec12a is required for the pathogenesis of NUP98::NSD1 AML.Blood advances · 2025Article
- Article
- Article
- Novel NUP98:TNRC18 fusion transcript in acute myeloid leukemia: a case report and literature review.Blood science (Baltimore, Md.) · 2025Article
- Review
- Transcriptional and epigenetic rewiring by the NUP98::KDM5A fusion oncoprotein directly activates CDK12.Nature communications · 2025Article
- Promising activity of Selinexor in the treatment of a patient with refractory NUP98-NSD1+/FLT3-ITD + acute myeloid leukemia.Annals of hematology · 2025Article
- From low remission to hope: the efficacy of targeted therapies in NUP98-R positive pediatric acute myeloid leukemia.World journal of pediatrics : WJP · 2025Article
- PROTAC-Mediated GSPT1 Degradation Impairs the Expression of Fusion Genes in Acute Myeloid Leukemia.Cancers · 2025Article
- Integrated single-cell and bulk RNA dequencing to identify and validate prognostic genes related to T Cell senescence in acute myeloid leukemia.Frontiers in bioinformatics · 2025Article
- Successful use of Palbociclib combined with Venetoclax and Azacitidine in an adult with refractory/relapsed therapy-related acute myeloid leukemia.Cancer chemotherapy and pharmacology · 2024Article
- NUP98 oncofusions in myeloid malignancies: An update on molecular mechanisms and therapeutic opportunities.HemaSphere · 2024Review
- Post-transcriptional regulation of DEAD-box RNA helicases in hematopoietic malignancies.Genes & diseases · 2024Review
- Combination of menin and kinase inhibitors as an effective treatment for leukemia with NUP98 translocations.Leukemia · 2024Article
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Authors and funding
27 authors at 10 institutions in 4 countries.
Funding
Abstract
Fusion proteins involving Nucleoporin 98 (NUP98) are recurrently found in acute myeloid leukemia (AML) and are associated with poor prognosis. Lack of mechanistic insight into NUP98-fusion-dependent oncogenic transformation has so far precluded the development of rational targeted therapies. We reasoned that different NUP98-fusion proteins deregulate a common set of transcriptional targets that might be exploitable for therapy. To decipher transcriptional programs controlled by diverse NUP98-fusion proteins, we developed mouse models for regulatable expression of NUP98/NSD1, NUP98/JARID1A, and NUP98/DDX10. By integrating chromatin occupancy profiles of NUP98-fusion proteins with transcriptome profiling upon acute fusion protein inactivation in vivo, we defined the core set of direct transcriptional targets of NUP98-fusion proteins. Among those, CDK6 was highly expressed in murine and human AML samples. Loss of CDK6 severely attenuated NUP98-fusion-driven leukemogenesis, and NUP98-fusion AML was sensitive to pharmacologic CDK6 inhibition in vitro and in vivo. These findings identify CDK6 as a conserved, critical direct target of NUP98-fusion proteins, proposing CDK4/CDK6 inhibitors as a new rational treatment option for AML patients with NUP98-fusions.
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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.