Evidence map›Paper›PMID 41571889›Full record

ArticleExperimental & molecular medicine2026

Switching off CK2-mediated activation of survivin offers new therapeutic opportunities in neuroblastoma.

Giulia Cazzanelli, Andrea Dalle Vedove, Francesca Broso, Matteo Burigotto, Jacopo Zasso, Giuseppe Aiello, Francesca Zonta, Andrea Astolfi, Maria Letizia Barreca, Maria Ruzzene and 4 more

Abstract read
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In one paragraph

Article in Experimental & molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Giulia CazzanelliDepartment of Cellular, Computational and Integrative Biology, University of Trento, Trento, Italy. giulia.cazzanelli@unitn.it.
Andrea Dalle VedoveDepartment of Cellular, Computational and Integrative Biology, University of Trento, Trento, Italy.
Francesca BrosoDepartment of Cellular, Computational and Integrative Biology, University of Trento, Trento, Italy.
Matteo BurigottoDepartment of Cellular, Computational and Integrative Biology, University of Trento, Trento, Italy.
Jacopo ZassoDepartment of Cellular, Computational and Integrative Biology, University of Trento, Trento, Italy.
Giuseppe AielloDepartment of Cellular, Computational and Integrative Biology, University of Trento, Trento, Italy.
Francesca ZontaDepartment of Biomedical Sciences and CNR Institute of Neuroscience, University of Padua, Padua, Italy.
Andrea AstolfiDepartment of Pharmaceutical Sciences, University of Perugia, Perugia, Italy.
Maria Letizia BarrecaDepartment of Pharmaceutical Sciences, University of Perugia, Perugia, Italy.ORCID http://orcid.org/0000-0003-3530-5042
Maria RuzzeneDepartment of Biomedical Sciences and CNR Institute of Neuroscience, University of Padua, Padua, Italy.
Luca TiberiDepartment of Cellular, Computational and Integrative Biology, University of Trento, Trento, Italy.ORCID http://orcid.org/0000-0002-5983-3782
Luca L FavaDepartment of Cellular, Computational and Integrative Biology, University of Trento, Trento, Italy.
Alessandro QuattroneDepartment of Cellular, Computational and Integrative Biology, University of Trento, Trento, Italy.
Graziano LolliDepartment of Cellular, Computational and Integrative Biology, University of Trento, Trento, Italy. graziano.lolli@unitn.it.ORCID http://orcid.org/0000-0002-8536-5599

Funding

Associazione Italiana per la Ricerca sul Cancro (Italian Association for Cancer Research) MFAG 2017 - ID. 19882Fondazione Umberto Veronesi (Umberto Veronesi Foundation) Postdoctoral Fellowship
6 · The paper itself

Abstract

CK2 is an antiapoptotic kinase overactive in various malignancies. Here we show that CK2 inhibition dramatically affects neuroblastoma growth both in vitro and in vivo. In particular, here we report on the identification of CK2-TN03, a CK2 inhibitor showing greater selectivity and cellular efficacy than silmitasertib, the only available clinical grade CK2 inhibitor with orphan status for cholangiocarcinoma and in clinical trials for medulloblastoma. CK2-TN03 acts by suppressing survivin, which is overexpressed in all high-risk neuroblastomas. Survivin function is affected by direct inhibition of its phosphorylation by CK2; its messenger RNA and protein levels are reduced through CK2 regulation of the MDM2/p53 balance via AKT1 and BRD4/MYCN. Accordingly, neuroblastoma cells persistently stall in mitosis before going to apoptosis. Finally, CK2-TN03 does not affect noncycling cells and significantly reduces tumor growth in mice xenografts without any apparent toxicity.

Indexed as

Antineoplastic AgentsCasein Kinase IIInhibitor of Apoptosis ProteinsNeuroblastomaProtein Kinase InhibitorsAnimalsApoptosisCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMicePhosphorylationProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mdm2SurvivinAntineoplastic AgentsBIRC5 protein, humanCasein Kinase IIInhibitor of Apoptosis ProteinsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mdm2SurvivinTumor Suppressor Protein p53

Identifiers

PMID41571889
PMCPMC12868639

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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.