ArticleScientific reports2026
CDK2 inhibition promotes neuronal differentiation in neuroblastoma.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
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Authors and funding
10 authors.
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Abstract
Neuroblastoma (NB) is a childhood tumor arising from neural crest-derived progenitor cells. Cyclin dependent kinase 2 (CDK2) has been suggested to be a promising therapeutic target in NB especially MYCN-amplified tumors. How CDK2 contributes to the development of NB is not fully understood. Here, we demonstrate that high CDK2 expression in NB correlates with advanced and high-risk disease, MYCN-amplification, poor prognosis, and undifferentiated tumors. We uncovered that CDK2 genetic or pharmacological inhibition induces neuronal differentiation in human NB cell lines, which effect is in general more prominent in the MYCN-amplified subtype. Further, we establish CDK2 as a MYCN target gene that modulate the MYC-pathway in MYCN-amplified NB. Notably, pharmacological inhibition of CDK2 in combination with MYCN inhibition or all-trans-retinoic acid (ATRA) differentiation therapy enhances neuronal differentiation in vitro. These results reveal an important function of CDK2 in NB and highlight CDK2 inhibition alone or in combination with MYC inhibitors and retinoids as a potential strategy for differentiation therapy in NB.
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