Evidence map›Paper›PMID 28888037›Full record

ArticleThe Journal of pathology2018

MYC drives overexpression of telomerase RNA (hTR/TERC) in prostate cancer.

Javier A Baena-Del Valle, Qizhi Zheng, David M Esopi, Michael Rubenstein, Gretchen K Hubbard, Maria C Moncaliano, Andrew Hruszkewycz, Ajay Vaghasia, Srinivasan Yegnasubramanian, Sarah J Wheelan and 4 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 2 pooled it
4.2field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

14 authors at 3 institutions in 2 countries.

Javier A Baena-Del ValleDepartment of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0001-8417-8946
Qizhi ZhengDepartment of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
David M EsopiSidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Michael RubensteinDepartment of Biological Sciences, University of Maryland, Baltimore County, Baltimore, Maryland, USA.
Gretchen K HubbardDepartment of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Maria C MoncalianoDepartment of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Andrew HruszkewyczDivision of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, Maryland, USA.
Ajay VaghasiaSidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Srinivasan YegnasubramanianSidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Sarah J WheelanSidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Alan K MeekerDepartment of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Christopher M HeaphyDepartment of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Mindy K GrahamDepartment of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Angelo M De MarzoDepartment of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Johns Hopkins University · USNational Cancer Institute · USUniversity of Maryland, Baltimore County · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI WILLIAM George NELSON · 1985 to 2026
$208.6M
TRANSGENIC MODELS FOR PROSTATE CANCER AND AUTOIMMUNITYP50CA058236 · NCI · JOHNS HOPKINS UNIVERSITY · PI DENMEADE, SAMUEL R · 1992 to 2020
$43.9M
TRAINING IN AREAS FUNDAMENTAL TO CANCER RESEARCHT32CA009110 · NCI · JOHNS HOPKINS UNIVERSITY · PI MATUNIS, MICHAEL J., WEERARATNA, ASHANI T · 1985 to 2025
$13.1M
Multidiciplinary Integrative Genomic Approach to Distinguish Lethal from Indolent Prostate Cancer in Men of Europena and African AncestryU01CA196390 · NCI · JOHNS HOPKINS UNIVERSITY · PI DE MARZO, ANGELO MICHAEL, PIENTA, KENNETH J. · 2015 to 2020
$5.8M
Establishing in vitro carcinoma models of the Alternative Lengthening of Telomeres pathway to elucidate molecular mechanisms and identify therapeutic vulnerabilitiesF32CA213742 · NCI · JOHNS HOPKINS UNIVERSITY · PI GRAHAM, MINDY KIM · 2017 to 2018
$118k
NCI NIH HHS F32 CA213742NCI NIH HHS P30 CA006973NCI NIH HHS P50 CA058236NCI NIH HHS U01 CA196390
6 · The paper itself

Abstract

Telomerase consists of at least two essential elements, an RNA component hTR or TERC that contains the template for telomere DNA addition and a catalytic reverse transcriptase (TERT). While expression of TERT has been considered the key rate-limiting component for telomerase activity, increasing evidence suggests an important role for the regulation of TERC in telomere maintenance and perhaps other functions in human cancer. By using three orthogonal methods including RNAseq, RT-qPCR, and an analytically validated chromogenic RNA in situ hybridization assay, we report consistent overexpression of TERC in prostate cancer. This overexpression occurs at the precursor stage (e.g. high-grade prostatic intraepithelial neoplasia or PIN) and persists throughout all stages of disease progression. Levels of TERC correlate with levels of MYC (a known driver of prostate cancer) in clinical samples and we also show the following: forced reductions of MYC result in decreased TERC levels in eight cancer cell lines (prostate, lung, breast, and colorectal); forced overexpression of MYC in PCa cell lines, and in the mouse prostate, results in increased TERC levels; human TERC promoter activity is decreased after MYC silencing; and MYC occupies the TERC locus as assessed by chromatin immunoprecipitation (ChIP). Finally, we show that knockdown of TERC by siRNA results in reduced proliferation of prostate cancer cell lines. These studies indicate that TERC is consistently overexpressed in all stages of prostatic adenocarcinoma and that its expression is regulated by MYC. These findings nominate TERC as a novel prostate cancer biomarker and therapeutic target. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedAnimalsCell ProliferationGenes, ReporterHumansIn Situ HybridizationMaleMiceMice, TransgenicMiddle AgedProstateProstatic Intraepithelial NeoplasiaProstatic NeoplasmsProto-Oncogene Proteins c-mycMYC protein, humanProto-Oncogene Proteins c-mycRNARNA, Small InterferingTelomerasetelomerase RNAMYCprostate carcinomaRNA in situ hybridizationtelomeraseTERC telomerase RNA component

Identifiers

PMID28888037
PMCPMC5801764
OpenAlexW2750776871

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.