Evidence map›Paper›PMID 39137728›Full record

ArticleCancer cell2024

Thyroid hormone suppresses medulloblastoma progression through promoting terminal differentiation of tumor cells.

Yijun Yang, Silvia Anahi Valdés-Rives, Qing Liu, Tong Gao, Chakkapong Burudpakdee, Yuzhe Li, Jun Tan, Yinfei Tan, Christian A Koch, Yuan Rong and 7 more

Abstract read
In one paragraph

Article in Cancer cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Article
  2. Article
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  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Summary of the Year in Review Lectures at the 2024 Annual Meeting of the American Thyroid Association.Thyroid : official journal of the American Thyroid Association · 2025
    Article
  11. Article
  12. Review
  13. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors.

Yijun YangNuclear Dynamics and Cancer Program, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA 19111, USA; Cancer Epigenetic Institute, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA 19111, USA.
Silvia Anahi Valdés-RivesNuclear Dynamics and Cancer Program, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA 19111, USA; Cancer Epigenetic Institute, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA 19111, USA.
Qing LiuDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Tong GaoCancer Signaling and Microenvironment Program, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA 19111, USA.
Chakkapong BurudpakdeeNuclear Dynamics and Cancer Program, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA 19111, USA; Cancer Epigenetic Institute, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA 19111, USA.
Yuzhe LiDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jun TanDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Yinfei TanDepartment of Pathology, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA 19111, USA.
Christian A KochDepartment of Medicine, Division of Endocrinology, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA 19111, USA.
Yuan RongDepartment of Pathology and Laboratory Medicine, Lewis Katz School of Medicine, Temple University Health System, Philadelphia, PA 19140, USA.
Steven R HouserCardiovascular Research Center, Lewis Katz School of Medicine, Temple University Health System, Philadelphia, PA 19140, USA.
Shuanzeng WeiDepartment of Pathology, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA 19111, USA.
Kathy Q CaiHistopathology Facility, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA 19111, USA.
Jinhua WuCancer Signaling and Microenvironment Program, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA 19111, USA.
Sheue-Yann ChengLaboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Robert Wechsler-ReyaBrain Tumor Research, Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY 10032, USA.
Zeng-Jie YangNuclear Dynamics and Cancer Program, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA 19111, USA; Cancer Epigenetic Institute, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA 19111, USA. Electronic address: zengjie.yang@fccc.edu.

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Dietmar J Kappes · 1985 to 2026
$138.8M
Novel Regulatory Mechanisms Underlying Inside-out Integrin ActivationR35GM119560 · NIGMS · RESEARCH INST OF FOX CHASE CAN CTR · PI Jinhua Wu · 2016 to 2026
$5.0M
Leukotriene-Induced Nestin Expression Promotes Medulloblastoma TumorigenesisR01CA178380 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI YANG, ZENG-JIE · 2014 to 2018
$1.9M
Fibroblasts Support the Growth of Brain Metastasis by Rendering Cancer Cells Resistant to Chemotherapy and Inducing Immunosuppression in Tumor MicroenvironmentR01CA276273 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Zeng-Jie Yang · 2023 to 2026
$1.6M
NCI NIH HHS P30 CA006927NCI NIH HHS R01 CA178380NCI NIH HHS R01 CA276273NIGMS NIH HHS R35 GM119560
6 · The paper itself

Abstract

Hypothyroidism is commonly detected in patients with medulloblastoma (MB). However, whether thyroid hormone (TH) contributes to MB pathogenicity remains undetermined. Here, we find that TH plays a critical role in promoting tumor cell differentiation. Reduction in TH levels frees the TH receptor, TRα1, to bind to EZH2 and repress expression of NeuroD1, a transcription factor that drives tumor cell differentiation. Increased TH reverses EZH2-mediated repression of NeuroD1 by abrogating the binding of EZH2 and TRα1, thereby stimulating tumor cell differentiation and reducing MB growth. Importantly, TH-induced differentiation of tumor cells is not restricted by the molecular subgroup of MB, suggesting that TH can be used to broadly treat MB subgroups. These findings establish an unprecedented association between TH signaling and MB pathogenicity, providing solid evidence for TH as a promising modality for MB treatment.

Indexed as

Basic Helix-Loop-Helix ProteinsCell DifferentiationEnhancer of Zeste Homolog 2 ProteinMedulloblastomaThyroid HormonesAnimalsCell Line, TumorCerebellar NeoplasmsDisease ProgressionGene Expression Regulation, NeoplasticHumansMiceSignal TransductionThyroid Hormone Receptors alphaBasic Helix-Loop-Helix ProteinsEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanNEUROD1 protein, humanThyroid Hormone Receptors alphaThyroid Hormonesdifferentiation therapyepigenetic regulationEZH2hypothyroidismmedulloblastomaNeuroD1terminal differentiationthyroid hormoneTRα1

Identifiers

PMID39137728
PMCPMC11565524

What OpenQuestion holds

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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 OpenQuestion graph.