Evidence map›Paper›PMID 34532611›Full record

ArticleAnnual review of cancer biology2021

Telomeres and Cancer: Resolving the Paradox.

Joe Nassour, Tobias T Schmidt, Jan Karlseder

Open access · hybridAbstract read
In one paragraph

Article in Annual review of cancer biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
6.5field-weighted citation impact, top 2% 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, 72 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Telomere Crisis Shapes Cancer Evolution.Cold Spring Harbor perspectives in biology · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. The Hallmarks of Aneuploidy in Cancer and Congenital Syndromes.Annual review of genomics and human genetics · 2025
    Review
  14. A mechanism for telomere-specific telomere length regulation.bioRxiv : the preprint server for biology · 2025
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  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

3 authors at 1 institution in 1 country.

Joe NassourMolecular and Cell Biology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.
Tobias T SchmidtMolecular and Cell Biology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.
Jan KarlsederMolecular and Cell Biology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.
Salk Institute for Biological Studies · US

Funding

Viral Vector Core (VVC)P30CA014195 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Ye Zheng · 1985 to 2026
$82.8M
Understanding the role of autophagy-regulated cell death in the escape from replicative crisisR01CA234047 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI KARLSEDER, JAN, SHAW, REUBEN · 2020 to 2024
$3.1M
Mitochondria-to-Nucleus Signaling in Colorectal CancerR01CA228211 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI HARGREAVES, DIANA CLARE, SHADEL, GERALD · 2020 to 2024
$2.6M
Understanding DNA break repair pathway choice regulation by the cNHEJ inhibitor CYRENR01CA227934 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI KARLSEDER, JAN · 2018 to 2022
$2.2M
The role of autophagy in the escape from replicative crisis and tumorigenesisK99CA252447 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI NASSOUR, JOE · 2020 to 2021
$326k
NCI NIH HHS K99 CA252447NCI NIH HHS P30 CA014195NCI NIH HHS R01 CA227934NCI NIH HHS R01 CA228211NCI NIH HHS R01 CA234047
6 · The paper itself

Abstract

Decades of study on cell cycle regulation have provided great insight into human cellular life span barriers, as well as their dysregulation during tumorigenesis. Telomeres, the extremities of linear chromosomes, perform an essential role in implementing these proliferative boundaries and preventing the propagation of potentially cancerous cells. The tumor-suppressive function of telomeres relies on their ability to initiate DNA damage signaling pathways and downstream cellular events, ranging from cell cycle perturbation to inflammation and cell death. While the tumor-suppressor role of telomeres is undoubtable, recent advances have pointed to telomeres as a major source of many of the genomic aberrations found in both early- and late-stage cancers, including the most recently discovered mutational phenomenon of chromothripsis. Telomere shortening appears as a double-edged sword that can function in opposing directions in carcinogenesis. This review focuses on the current knowledge of the dual role of telomeres in cancer and suggests a new perspective to reconcile the paradox of telomeres and their implications in cancer etiology.

Indexed as

genome instabilityproliferative life span barriersreplicative crisisreplicative senescencetelomeretumorigenesis

Identifiers

PMID34532611
PMCPMC8442540
OpenAlexW3135742164

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.