Evidence map›Paper›PMID 42680848›Full record

ReviewNature reviews. Genetics2026

How telomere attrition protects against cancer.

Alexander Stuart, Bokai Zhang, Dirk Hockemeyer, Titia de Lange

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

4 authors.

Alexander StuartLaboratory of Cell Biology and Genetics, Rockefeller University, New York, NY, USA.ORCID http://orcid.org/0000-0002-0355-2471
Bokai ZhangLaboratory of Cell Biology and Genetics, Rockefeller University, New York, NY, USA.ORCID http://orcid.org/0000-0003-1854-0227
Dirk HockemeyerDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA. hockemeyer@berkeley.edu.
Titia de LangeLaboratory of Cell Biology and Genetics, Rockefeller University, New York, NY, USA. delange@rockefeller.edu.ORCID http://orcid.org/0000-0002-9267-367X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have shown that telomere attrition functions as a powerful and broadly effective tumour-suppressor mechanism that halts emerging cancers when telomeric DNA becomes depleted. This Review highlights new insights into how telomere attrition guards against cancer, including its role in limiting cell proliferation, the importance of telomere length at birth for lifelong cancer prevention, the mechanisms governing telomere length regulation and how telomerase activation enables malignant cells to bypass this barrier. In contrast to the popular perception that telomere shortening is harmful, the findings demonstrate that normal telomere attrition limits the risk of cancer and suggest that counteracting telomere attrition in healthy individuals (for example, by activating telomerase) could enable tumour outgrowth. Thus, such interventions are best reserved for patients with diseases caused by excessively short telomeres. The new data also further underscore the promise of telomerase inhibition as a broadly effective cancer therapy.

Identifiers

What OpenQuestion holds

Textmetadata
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.