Evidence map›Paper›PMID 26158413›Full record

ArticleOncotarget2015

TCF21 hypermethylation in genetically quiescent clear cell sarcoma of the kidney.

Saskia L Gooskens, Samantha Gadd, Jaime M Guidry Auvil, Daniela S Gerhard, Javed Khan, Rajesh Patidar, Daoud Meerzaman, Qing-Rong Chen, Chih Hao Hsu, Chunhua Yan and 11 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.6field-weighted citation impact, top 7% of its field
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

23 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Pathway Analysis for Cancer Research and Precision Oncology Applications.Advances in experimental medicine and biology · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Role of the bHLH transcription factor TCF21 in development and tumorigenesis.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021
    Review
  10. TCF21: a critical transcription factor in health and cancer.Journal of molecular medicine (Berlin, Germany) · 2020
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Transcription Factor 21 (TCF21) rs12190287 Polymorphism is Associated with Osteosarcoma Risk and Outcomes in East Chinese Population.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 8 institutions in 2 countries.

Saskia L GooskensDepartment of Pediatric Hematology and Oncology, Erasmus MC - Sophia Children's Hospital, Rotterdam, The Netherlands.
Samantha GaddDepartment of Pathology, Ann and Robert H. Lurie Children's Hospital of Chicago, Northwestern University's Feinberg School of Medicine and Robert H. Lurie Cancer Center, Chicago, IL, USA.
Jaime M Guidry AuvilOffice of Cancer Genomics, National Cancer Institute, Bethesda, MD, USA.
Daniela S GerhardOffice of Cancer Genomics, National Cancer Institute, Bethesda, MD, USA.
Javed KhanGenetics Branch, Oncogenomics section, National Cancer Institute, Bethesda, MD, USA.
Rajesh PatidarGenetics Branch, Oncogenomics section, National Cancer Institute, Bethesda, MD, USA.
Daoud MeerzamanComputational Genomics Research Group, Center for Biomedical Informatics and Information Technology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Qing-Rong ChenComputational Genomics Research Group, Center for Biomedical Informatics and Information Technology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Chih Hao HsuComputational Genomics Research Group, Center for Biomedical Informatics and Information Technology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Chunhua YanComputational Genomics Research Group, Center for Biomedical Informatics and Information Technology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Cu NguyenComputational Genomics Research Group, Center for Biomedical Informatics and Information Technology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Ying HuComputational Genomics Research Group, Center for Biomedical Informatics and Information Technology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Charles G MullighanDepartment of Pathology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Jing MaDepartment of Pathology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Lawrence J JenningsDepartment of Pathology, Ann and Robert H. Lurie Children's Hospital of Chicago, Northwestern University's Feinberg School of Medicine and Robert H. Lurie Cancer Center, Chicago, IL, USA.
Ronald R de KrijgerDepartment of Pathology, Josephine Nefkens Institute, Erasmus MC, Rotterdam, The Netherlands.
Marry M van den Heuvel-EibrinkDepartment of Pediatric Oncology, Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands.
Malcolm A SmithCancer Therapy Evaluation Program, National Cancer Institute, Bethesda, MD, USA.
Nicole RossDepartment of Pathology and Laboratory Medicine, Nationwide Children's Hospital, Ohio State University College of Medicine, Columbus, OH, USA.
Julie M Gastier-FosterDepartment of Pathology and Laboratory Medicine, Nationwide Children's Hospital, Ohio State University College of Medicine, Columbus, OH, USA.
Elizabeth J PerlmanDepartment of Pathology, Ann and Robert H. Lurie Children's Hospital of Chicago, Northwestern University's Feinberg School of Medicine and Robert H. Lurie Cancer Center, Chicago, IL, USA.
National Institutes of Health · USNational Cancer Institute · USLurie Children's Hospital · USNationwide Children's Hospital · USPrincess Máxima Center · NLSt. Jude Children's Research Hospital · USMeertens Institute · NLRobert H. Lurie Comprehensive Cancer Center of Northwestern University

Funding

COG FOREIGN ACCRUALU10CA098543 · NCI · NATIONAL CHILDHOOD CANCER FOUNDATION · PI ADAMSON, PETER C. · 2003 to 2013
$335.5M
Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
Support for Human Specimen Banking in NCI-Supported Cancer Clinical TrialsU24CA114766 · NCI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI RAMIREZ MILAN, NILSA DEL CARMEN · 2005 to 2014
$14.5M
Therapy Resistance Mechanisms for CancerZIABC010998 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KHAN, JAVED · 2009 to 2025
$14.5M
NWTSG Foreign AccrualU10CA042326 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI GREEN, DANIEL MICHAEL · 1985 to 2003
$2.8M
CATEGORIZATION OF WILMS TUMOR BY GENETIC EXPRESSIONU01CA088131 · NCI · LURIE CHILDREN'S HOSPITAL OF CHICAGO · PI PERLMAN, ELIZABETH J · 2001 to 2006
$1.7M
CCR NIH HHS HHSN261200800001CNCI NIH HHS HHSN261200800001ENCI NIH HHS P30 CA060553NCI NIH HHS U01 CA088131NCI NIH HHS U10 CA098543NCI NIH HHS U10CA42326NCI NIH HHS U10CA88131NCI NIH HHS U10 CA98543NCI NIH HHS U10CA98543NCI NIH HHS U24 CA114766NCI NIH HHS U24CA114766
6 · The paper itself

Abstract

Clear Cell Sarcoma of the Kidney (CCSK) is a rare childhood tumor whose molecular pathogenesis remains poorly understood. We analyzed a discovery set of 13 CCSKs for changes in chromosome copy number, mutations, rearrangements, global gene expression and global DNA methylation. No recurrent segmental chromosomal copy number changes or somatic variants (single nucleotide or small insertion/deletion) were identified. One tumor with t(10;17)(q22;p13) involving fusion of YHWAE with NUTM2B was identified. Integrated analysis of expression and methylation data identified promoter hypermethylation and low expression of the tumor suppressor gene TCF21 (Pod-1/capsulin/epicardin) in all CCSKs except the case with t(10;17)(q22;p13). TARID, the long noncoding RNA responsible for demethylating TCF21, was virtually undetectable in most CCSKs. TCF21 hypermethylation and decreased TARID expression were validated in an independent set of CCSK tumor samples. The presence of significant hypermethylation of TCF21, a transcription factor known to be active early in renal development, supports the hypothesis that hypermethylation of TCF21 and/or decreased TARID expression lies within the pathogenic pathway of most CCSKs. Future studies are needed to functionally verify a tumorigenic role of TCF21 down-regulation and to tie this to the unique gene expression pattern of CCSK.

Indexed as

DNA MethylationBasic Helix-Loop-Helix ProteinsDNA Copy Number VariationsGene ExpressionHumansKidney NeoplasmsPolymorphism, Single NucleotidePromoter Regions, GeneticSarcoma, Clear CellBasic Helix-Loop-Helix ProteinsTCF21 protein, humanclear cell sarcoma of the kidneymethylationTARIDTCF21whole genome sequencing

Identifiers

PMID26158413
PMCPMC4599240
OpenAlexW1592922493

What OpenQuestion holds

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Registered trials

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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.