Evidence map›Paper›PMID 23776040›Full record

ArticleCancer discovery2013

ZNF365 promotes stability of fragile sites and telomeres.

Yuqing Zhang, Sandra J Shin, Debra Liu, Elena Ivanova, Friedrich Foerster, Haoqiang Ying, Hongwu Zheng, Yonghong Xiao, Zhengming Chen, Alexei Protopopov and 2 more

Open access · greenAbstract read
In one paragraph

Article in Cancer discovery, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

  1. Inflammatory bowel disease and breast cancer: epidemiological evidence, shared biology, and clinical management.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  5. Potential Role of Zinc Finger 365Iranian journal of medical sciences · 2023
    Article
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  8. Telomere maintenance in African trypanosomes.Frontiers in molecular biosciences · 2023
    Review
  9. Article
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  14. Article
  15. Article
  16. Article
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  18. Article
  19. 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

12 authors at 4 institutions in 1 country.

Yuqing ZhangDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, USA.
Sandra J Shin
Debra Liu
Elena Ivanova
Friedrich Foerster
Haoqiang Ying
Hongwu Zheng
Yonghong Xiao
Zhengming Chen
Alexei Protopopov
Ronald A Depinho
Ji-Hye Paik
The University of Texas MD Anderson Cancer Center · USCold Spring Harbor Laboratory · USCornell University · USDana-Farber Cancer Institute · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Clinical and Translational Science CenterUL1TR000457 · NCATS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IMPERATO-MCGINLEY, JULIANNE L · 2012 to 2016
$46.0M
TELOMERASE IN DEVELOPMENT, SENESCENCE AND NEOPLASIAR01CA084628 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DEPINHO, RONALD ANTHONY · 2000 to 2019
$10.5M
Uses of GEM models for Translational Cancer ResearchU01CA141508 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI CHIN, LYNDA · 2009 to 2013
$3.9M
Telomerase in Development, Senescence and NeoplasiaR37CA084628 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DEPINHO, RONALD ANTHONY · 2013 to 2014
$1.2M
NCATS NIH HHS UL1 TR000457NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA084628NCI NIH HHS R01CA84628NCI NIH HHS R37 CA084628NCI NIH HHS U01 CA141508NCI NIH HHS U01CA141508NIA NIH HHS AG-NS-0646-10
6 · The paper itself

Abstract

Critically short telomeres activate cellular senescence or apoptosis, as mediated by the tumor suppressor p53, but in the absence of this checkpoint response, telomere dysfunction engenders chromosomal aberrations and cancer. Here, analysis of p53-regulated genes activated in the setting of telomere dysfunction identified Zfp365 (ZNF365 in humans) as a direct p53 target that promotes genome stability. Germline polymorphisms in the ZNF365 locus are associated with increased cancer risk, including those associated with telomere dysfunction. On the mechanistic level, ZNF365 suppresses expression of a subset of common fragile sites, including telomeres. In the absence of ZNF365, defective telomeres engage in aberrant recombination of telomere ends, leading to increased telomere sister chromatid exchange and formation of anaphase DNA bridges, including ultra-fine DNA bridges, and ultimately increased cytokinesis failure and aneuploidy. Thus, the p53-ZNF365 axis contributes to genomic stability in the setting of telomere dysfunction.

Indexed as

Cellular SenescenceChromosome AberrationsChromosome Fragile SitesDNA-Binding ProteinsDNA DamageGenomic InstabilityHumansNeoplasmsTelomereTranscription FactorsTumor Suppressor Protein p53DNA-Binding ProteinsTP53 protein, humanTranscription FactorsTumor Suppressor Protein p53ZNF365 protein, human

Identifiers

PMID23776040
PMCPMC3710545
OpenAlexW2116571968

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.