Evidence map›Paper›PMID 42793176›Full record

ReviewBiomolecules2026

Beyond End Protection: Shelterin, POT1 Dysfunction, and Telomere Replication Stress in Cancer.

Tadahiko Matsumoto, Akifumi Takaori-Kondo

Abstract readReview
In one paragraph

Review in Biomolecules, 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

2 authors.

Tadahiko MatsumotoDepartment of Hematology, Graduate School of Medicine, Kyoto University, Kyoto 606-8303, Japan.
Akifumi Takaori-KondoDepartment of Hematology, Graduate School of Medicine, Kyoto University, Kyoto 606-8303, Japan.ORCID 0000-0001-7678-4284

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Telomeres (chromosome-end nucleoprotein complexes) are prone to replication fork stalling because of their G-rich repetitive sequences, G-quadruplexes, t-loops, oxidative lesions, and telomeric R-loops generated when telomeric repeat-containing RNA (TERRA) hybridizes with telomeric DNA. In this review, we will summarize how telomeres are replicated and maintained and the mechanisms by which replication stress occurs at telomeres. Subsequently, we will review the role of POT1 mutations in cancer development and pathology and discuss therapeutic strategies targeting telomere biology in cancer.

Indexed as

DNA ReplicationNeoplasmsShelterin ComplexTelomereTelomere-Binding ProteinsAnimalsHumansMutationPOT1 protein, humanShelterin ComplexTelomere-Binding ProteinsALTcancerPOT1replication stresstelomerasetelomere

Identifiers

PMID42793176
PMCPMC13604779

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.