Evidence map›Paper›PMID 33828097›Full record

ArticleNature communications2021

Structural variant evolution after telomere crisis.

Sally M Dewhurst, Xiaotong Yao, Joel Rosiene, Huasong Tian, Julie Behr, Nazario Bosco, Kaori K Takai, Titia de Lange, Marcin Imieliński

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.1field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. How telomere attrition protects against cancer.Nature reviews. Genetics · 2026
    Review
  2. Article
  3. Article
  4. Micronuclei: origins, assays, mechanisms, diseases and treatments.Signal transduction and targeted therapy · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Chromothripsis in cancer.Nature reviews. Cancer · 2025
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

9 authors at 3 institutions in 2 countries.

Sally M Dewhurst *Laboratory of Cell Biology and Genetics, Rockefeller University, New York, NY, USA.
Xiaotong Yao *Tri-Institutional Ph.D. Program in Computational Biology and Medicine, Weill Cornell Medicine, New York, NY, USA.
Joel RosieneDepartment of Pathology and Laboratory Medicine, Englander Institute for Precision Medicine, Institute for Computational Biomedicine, and Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA.
Huasong TianDepartment of Pathology and Laboratory Medicine, Englander Institute for Precision Medicine, Institute for Computational Biomedicine, and Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA.
Julie BehrTri-Institutional Ph.D. Program in Computational Biology and Medicine, Weill Cornell Medicine, New York, NY, USA.
Nazario BoscoLaboratory of Cell Biology and Genetics, Rockefeller University, New York, NY, USA.
Kaori K TakaiLaboratory of Cell Biology and Genetics, Rockefeller University, New York, NY, USA.
Titia de LangeLaboratory of Cell Biology and Genetics, Rockefeller University, New York, NY, USA. delange@rockefeller.edu.ORCID 0000-0002-9267-367X
Marcin ImielińskiDepartment of Pathology and Laboratory Medicine, Englander Institute for Precision Medicine, Institute for Computational Biomedicine, and Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA. mski@mskilab.org.ORCID 0000-0002-2211-4741
Cornell University · USRockefeller University · USNYU Langone Health · US

Funding

MECHANISMS OF TELOMERE INDUCED SENESCENCER01AG016642 · NIA · ROCKEFELLER UNIVERSITY · PI Titia de Lange · 1999 to 2026
$11.9M
Genome instability in cancer: telomeres and DNA repairR35CA210036 · NCI · ROCKEFELLER UNIVERSITY · PI Titia de Lange · 2016 to 2026
$10.8M
NCI NIH HHS R35 CA210036NIA NIH HHS R01 AG016642
6 · The paper itself

Abstract

Telomere crisis contributes to cancer genome evolution, yet only a subset of cancers display breakage-fusion-bridge (BFB) cycles and chromothripsis, hallmarks of experimental telomere crisis identified in previous studies. We examine the spectrum of structural variants (SVs) instigated by natural telomere crisis. Eight spontaneous post-crisis clones did not show prominent patterns of BFB cycles or chromothripsis. Their crisis-induced genome rearrangements varied from infrequent simple SVs to more frequent and complex SVs. In contrast, BFB cycles and chromothripsis occurred in MRC5 fibroblast clones that escaped telomere crisis after CRISPR-controlled telomerase activation. This system revealed convergent evolutionary lineages altering one allele of chromosome 12p, where a short telomere likely predisposed to fusion. Remarkably, the 12p chromothripsis and BFB events were stabilized by independent fusions to chromosome 21. The data establish that telomere crisis can generate a wide spectrum of SVs implying that a lack of BFB patterns and chromothripsis in cancer genomes does not indicate absence of past telomere crisis.

Indexed as

ChromothripsisCell LineChromosomal InstabilityFibroblastsGenomeGenomic InstabilityHumansLungMetaphaseModels, BiologicalNeoplasmsTelomere

Identifiers

PMID33828097
PMCPMC8027843
OpenAlexW3151221303

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.