Evidence map›Paper›PMID 41001593›Full record

ArticleMolecular & cellular oncology2025

Loss of Schwann cell's normal rhythmic core clock gene expression and gain of rhythmic expression of oncogenic driver genes in malignant NF1-associated peripheral nerve sheath tumor.

Sandra Leisz, Antonio Pelligrino, Saskia Fritzsche, Merle Wiegers, Markus Wösle, Christian Linke, Swanhild Lohse, Daniel Tippner, Christian Scheller, Christian Strauss and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular & cellular oncology, 2025. 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

15 authors.

Sandra LeiszDepartment of Neurosurgery, University Medicine Halle, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.ORCID https://orcid.org/0000-0003-4581-5185
Antonio PelligrinoFraunhofer Institute for Cell Therapy and Immunology, Branch Bioanalytics and Bioprocesses, Potsdam, Germany.
Saskia FritzscheDepartment of Neurosurgery, University Medicine Halle, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Merle WiegersDepartment of Neurosurgery, University Medicine Halle, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Markus WösleClinic for Radiotherapy and Radiation Oncology, Dessau City Hospital, Dessau-Roßlau, Germany.
Christian LinkeDepartment of Hematology and Oncology, Center for Translational Medicine, University Hospital Brandenburg, Brandenburg Medical School Theodor Fontane, Brandenburg an der Havel, Germany.
Swanhild LohseCURE-NF Research Group, Medical Faculty, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Daniel TippnerCURE-NF Research Group, Medical Faculty, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Christian SchellerDepartment of Neurosurgery, University Medicine Halle, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Christian StraussDepartment of Neurosurgery, University Medicine Halle, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Eva Ehrentreich-FörsterFraunhofer Institute for Cell Therapy and Immunology, Branch Bioanalytics and Bioprocesses, Potsdam, Germany.
Faramarz DehghaniDepartment of Anatomy and Cell Biology, Medical Faculty, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Stanislav SysInstitute for Developmental Biology and Neurobiology, and Institute of Human Genetics, University Medical Center Johannes Gutenberg University (UMC), Mainz, Germany.
Erik MarondeInstitute for Anatomy II, Faculty of Medicine, Goethe University Frankfurt, Frankfurt (Main), Germany.
Anja HarderCURE-NF Research Group, Medical Faculty, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurofibromatosis type 1 (NF1) is an autosomal dominant tumor syndrome caused by pathogenic variants in the

Indexed as

Circadianclock geneMPNSTNF1rhythmSchwann cell

Identifiers

PMID41001593
PMCPMC12459363

What Socratic holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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 Socratic graph.