Evidence map›Paper›PMID 39620202›Full record

ArticleNeuro-oncology advances

Multiomic analyses reveal new targets of polycomb repressor complex 2 in Schwann lineage cells and malignant peripheral nerve sheath tumors.

Minu M Bhunia, Christopher M Stehn, Tyler A Jubenville, Ethan L Novacek, Alex T Larsson, Mahathi Madala, Suganth Suppiah, Germán L Velez-Reyes, Kyle B Williams, Mark Sokolowski and 10 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuro-oncology advances. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
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

20 authors.

Minu M BhuniaDepartment of Genetics, Cell Biology and Development, University of Minnesota, Twin Cities, Minneapolis, Minnesota, USA.ORCID https://orcid.org/0000-0002-2849-1572
Christopher M StehnDepartment of Genetics, Cell Biology and Development, University of Minnesota, Twin Cities, Minneapolis, Minnesota, USA.ORCID https://orcid.org/0000-0003-2911-1954
Tyler A JubenvilleDepartment of Pediatrics, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA.ORCID https://orcid.org/0009-0003-9578-4847
Ethan L NovacekDepartment of Pediatrics, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA.ORCID https://orcid.org/0009-0000-9685-7196
Alex T LarssonDepartment of Pediatrics, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA.ORCID https://orcid.org/0000-0002-1350-8271
Mahathi MadalaDepartment of Pediatrics, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA.
Suganth SuppiahMacFeeters-Hamilton Center for Neuro-Oncology, Princess Margaret Cancer Center, Toronto, Ontario, Canada.ORCID https://orcid.org/0000-0003-4569-0466
Germán L Velez-ReyesDepartment of Pediatrics, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA.ORCID https://orcid.org/0000-0001-8510-8667
Kyle B WilliamsDepartment of Pediatrics, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA.ORCID https://orcid.org/0000-0003-4333-9111
Mark SokolowskiDepartment of Pediatrics, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA.ORCID https://orcid.org/0000-0002-2385-5373
Rory L WilliamsDepartment of Pediatrics, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA.ORCID https://orcid.org/0000-0003-2605-5790
Samuel J FinnertyDepartment of Genetics, Cell Biology and Development, University of Minnesota, Twin Cities, Minneapolis, Minnesota, USA.
Nuri A TemizDepartment of Pediatrics, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA.ORCID https://orcid.org/0000-0003-1416-3639
Ariel CarideEpigenomics Development Laboratory, Epigenomics Program, Center for Individualized Medicine, Mayo Clinic, Rochester, Minnesota, USA.ORCID https://orcid.org/0000-0002-1642-6837
Aditya V BhagwateDepartment of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, Minnesota, USA.ORCID https://orcid.org/0000-0003-0192-9594
Nagaswaroop K NagarajDepartment of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, Minnesota, USA.ORCID https://orcid.org/0000-0002-4442-2585
Jeong-Heon LeeEpigenomics Development Laboratory, Epigenomics Program, Center for Individualized Medicine, Mayo Clinic, Rochester, Minnesota, USA.
Tamas OrdogEpigenomics Development Laboratory, Epigenomics Program, Center for Individualized Medicine, Mayo Clinic, Rochester, Minnesota, USA.ORCID https://orcid.org/0000-0002-3940-7284
Gelareh ZadehMacFeeters-Hamilton Center for Neuro-Oncology, Princess Margaret Cancer Center, Toronto, Ontario, Canada.ORCID https://orcid.org/0000-0002-6637-4502
David A LargaespadaDepartment of Genetics, Cell Biology and Development, University of Minnesota, Twin Cities, Minneapolis, Minnesota, USA.ORCID https://orcid.org/0000-0002-3183-0491

Funding

Uncovering treatment targets for peripheral nerve sheath tumor progression in NF1R01NS115438 · NINDS · UNIVERSITY OF MINNESOTA · PI LARGAESPADA, DAVID ANDREW, RATNER, NANCY · 2020 to 2024
$2.9M
Disordered Regulation of Wnt/beta-catenin Signaling in MPNST Development and MaintenanceR01NS086219 · NINDS · UNIVERSITY OF MINNESOTA · PI LARGAESPADA, DAVID ANDREW, RATNER, NANCY · 2014 to 2018
$2.4M
NINDS NIH HHS R01 NS086219NINDS NIH HHS R01 NS115438
6 · The paper itself

Abstract

Background: Malignant peripheral nerve sheath tumors (MPNSTs) can arise from atypical neurofibromas (ANF). Loss of the polycomb repressor complex 2 (PRC2) is a common event. Previous studies on PRC2-regulated genes in MPNST used genetic add-back experiments in highly aneuploid MPNST cell lines which may miss PRC2-regulated genes in Methods: We engineered Results: We identified potential PRC2-regulated drivers of MPNST progression. Pathway analysis indicates many upregulated cancer-related pathways. We found transcriptional evidence for activated Notch and Sonic Hedgehog (SHH) signaling in PRC2-deficient iHSCs. Functional studies confirm that Notch signaling is active in MPNST cell lines, patient-derived xenografts, and transient cell models of PRC2 deficiency. A combination of MEK and γ-secretase inhibition shows synergy in MPNST cell lines. Conclusions: We identified PRC2-regulated genes and potential drivers of MPNSTs. Our findings support the Notch pathway as a druggable target in MPNSTs. Our identification of PRC2-regulated genes and pathways could result in more novel therapeutic approaches.

Indexed as

MPNSTNF1nirogacestatnotch signalingPRC2

Identifiers

PMID39620202
PMCPMC11606644

What Socratic holds

Textmetadata
LicenceCC BY
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.