Evidence map›Paper›PMID 29874588›Full record

ArticleCell reports2018

Administration of a Nucleoside Analog Promotes Cancer Cell Death in a Telomerase-Dependent Manner.

Xuehuo Zeng, Wilnelly Hernandez-Sanchez, Mengyuan Xu, Tawna L Whited, Diane Baus, Junran Zhang, Anthony J Berdis, Derek J Taylor

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Telomere Reprogramming and Cellular Metabolism: Is There a Link?International journal of molecular sciences · 2024
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Telomere Targeting Approaches in Cancer: Beyond Length Maintenance.International journal of molecular sciences · 2022
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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

8 authors at 2 institutions in 1 country.

Xuehuo ZengDepartment of Pharmacology, Case Western Reserve University, Cleveland, OH 44106, USA.
Wilnelly Hernandez-SanchezDepartment of Pharmacology, Case Western Reserve University, Cleveland, OH 44106, USA.
Mengyuan XuDepartment of Pharmacology, Case Western Reserve University, Cleveland, OH 44106, USA.
Tawna L WhitedDepartment of Pharmacology, Case Western Reserve University, Cleveland, OH 44106, USA.
Diane BausDepartment of Pharmacology, Case Western Reserve University, Cleveland, OH 44106, USA.
Junran ZhangDepartment of Radiation Oncology, Case Western Reserve University, Cleveland, OH 44106, USA.
Anthony J BerdisDepartment of Chemistry, Cleveland State University, Cleveland, OH 44115, USA.
Derek J TaylorDepartment of Pharmacology, Case Western Reserve University, Cleveland, OH 44106, USA; Department of Biochemistry, Case Western Reserve University, Cleveland, OH 44106, USA. Electronic address: derek.taylor@case.edu.
Case Western Reserve University · USCleveland State University · US

Funding

Induction of cancer cell death by selective DNA misincorporationDP2CA186571 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI TAYLOR, DEREK JAMES · 2013 to 2014
$2.6M
THE ROLE OF NEDD4-1 IN IGF-1R SIGNALINGR01CA154625 · NCI · WASHINGTON UNIVERSITY · PI ZHANG, JUNRAN · 2011 to 2016
$1.6M
NCI NIH HHS DP2 CA186571NCI NIH HHS R01 CA154625
6 · The paper itself

Abstract

Telomerase, the end-replication enzyme, is reactivated in malignant cancers to drive cellular immortality. While this distinction makes telomerase an attractive target for anti-cancer therapies, most approaches for inhibiting its activity have been clinically ineffective. As opposed to inhibiting telomerase, we use its activity to selectively promote cytotoxicity in cancer cells. We show that several nucleotide analogs, including 5-fluoro-2'-deoxyuridine (5-FdU) triphosphate, are effectively incorporated by telomerase into a telomere DNA product. Administration of 5-FdU results in an increased number of telomere-induced foci, impedes binding of telomere proteins, activates the ATR-related DNA-damage response, and promotes cell death in a telomerase-dependent manner. Collectively, our data indicate that telomerase activity can be exploited as a putative anti-cancer strategy.

Indexed as

AminopeptidasesCell DeathCell Line, TumorDeoxyuridineDipeptidyl-Peptidases and Tripeptidyl-PeptidasesDNADNA DamageGene SilencingHEK293 CellsHumansModels, BiologicalNeoplasmsNuclear ProteinsNucleosidesProtein BindingPyrimidines5-formyl-2'-deoxyuridineAminopeptidasesDeoxyuridineDipeptidyl-Peptidases and Tripeptidyl-PeptidasesDNANuclear ProteinsNucleosidesPOT1 protein, humanpyrimidinePyrimidinesRNA, Small InterferingSerine ProteasesShelterin ComplexTelomeraseTelomere-Binding ProteinsThymidineTripeptidyl-Peptidase 15-fluoro-2'-deoxyuridineDNA damagefloxuridinePOT1telomerasetelomere

Identifiers

PMID29874588
PMCPMC6072277
OpenAlexW2807683045

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.