Evidence map›Paper›PMID 34861996›Full record

ReviewSeminars in radiation oncology2022

Chromosome Missegregation as a Modulator of Radiation Sensitivity.

Pippa F Cosper, Sarah E Copeland, John B Tucker, Beth A Weaver

Abstract readReview
In one paragraph

Review in Seminars in radiation oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed.

  1. Article
  2. Pretreatment Chromosomal Instability Correlates With Radiation Sensitivity in Squamous Cell Cancers.International journal of radiation oncology, biology, physics · 2026
    Article
  3. Article
  4. Article
  5. Biomedicines · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Interferon Epsilon Loss Is Elusive 9p21 Link to Immune-Cold Tumors, Resistant to Immune Checkpoint Therapy, and Endogenous CXCL9/10 Induction.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2025
    Review
  12. Review
  13. Article
  14. Article
  15. Microtubule poleward flux as a target for modifying chromosome segregation errors.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. The two sides of chromosomal instability: drivers and brakes in cancer.Signal transduction and targeted therapy · 2024
    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

4 authors.

Pippa F CosperDepartment of Human Oncology, Madison, WI; University of Wisconsin Carbone Cancer Center, Madison, WI.
Sarah E CopelandMolecular & Cellular Pharmacology Graduate Training Program, Madison, WI.
John B TuckerCancer Biology Graduate Training Program, Madison, WI.
Beth A WeaverUniversity of Wisconsin Carbone Cancer Center, Madison, WI; Department of Cellular and Regenerative Biology, Madison, WI; Department of Oncology/McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI.. Electronic address: baweaver@wisc.edu.

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Christian Capitini · 1985 to 2026
$142.6M
Training in Cancer Biology Training GrantT32CA009135 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI SUGDEN, WILLIAM M. · 1985 to 2024
$10.4M
Training Program In Molecular AND Cellular PharmacologyT32GM008688 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI AUDHYA, ANJON · 1998 to 2020
$6.0M
Impact of chromosomal instability on sensitivity to microtubule-targeting drugs in breast cancerR01CA234904 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI BURKARD, MARK E, WEAVER, BETH A · 2019 to 2023
$2.7M
NCI NIH HHS P30 CA014520NCI NIH HHS R01 CA234904NCI NIH HHS T32 CA009135NIGMS NIH HHS T32 GM008688
6 · The paper itself

Abstract

Chromosome missegregation over the course of multiple cell divisions, termed chromosomal instability (CIN), is a hallmark of cancer. Multiple causes of CIN have been identified, including defects in the mitotic checkpoint, altered kinetochore-microtubule dynamics, centrosome amplification, and ionizing radiation. Here we review the types, mechanisms, and cellular implications of CIN. We discuss the evidence that CIN can promote tumors, suppress them, or do neither, depending on the rates of chromosome missegregration and the cellular context. Very high rates of chromosome missegregation lead to cell death due to loss of essential chromosomes; thus elevating CIN above a tolerable threshold provides a mechanistic opportunity to promote cancer cell death. Lethal rates of CIN can be achieved by a single insult or through a combination of insults. Because ionizing radiation induces CIN, additional therapies that increase CIN may serve as useful modulators of radiation sensitivity. Ultimately, quantifying the intrinsic CIN in a tumor and modulating this level pharmacologically as well as with radiation may allow for a more rational, personalized radiation therapy prescription, thereby decreasing side effects and increasing local control.

Indexed as

Chromosome SegregationNeoplasmsCentrosomeChromosomal InstabilityHumansKinetochoresRadiation Tolerance

Identifiers

PMID34861996
PMCPMC8883596

What OpenQuestion holds

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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.