Evidence map›Paper›PMID 23416057›Full record

ArticleSeminars in cell & developmental biology2013

2n or not 2n: Aneuploidy, polyploidy and chromosomal instability in primary and tumor cells.

Lauren M Zasadil, Eric M C Britigan, Beth A Weaver

Abstract read
In one paragraph

Article in Seminars in cell & developmental biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing 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

64 citing papers in PubMed.

  1. Review
  2. Article
  3. Pretreatment Chromosomal Instability Correlates With Radiation Sensitivity in Squamous Cell Cancers.International journal of radiation oncology, biology, physics · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Docetaxel response in BRCA1,p53-deficient mammary tumor cells is affected by Huntingtin and BAP1.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  8. Review
  9. Article
  10. Review
  11. The two sides of chromosomal instability: drivers and brakes in cancer.Signal transduction and targeted therapy · 2024
    Review
  12. Review
  13. The reckoning of chromosomal instability: past, present, future.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2024
    Review
  14. Review
  15. Chromosome instability and aneuploidy in the mammalian brain.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

4 more citing papers are in PubMed but not listed here.

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.

Lauren M ZasadilDepartment of Cell and Regenerative Biology, University of Wisconsin, Madison, WI 53705, USA.
Eric M C Britigan
Beth A Weaver

Funding

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
Mitosis, Aneuploidy and CancerR01CA140458 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI WEAVER, BETH A · 2011 to 2015
$1.5M
NCI NIH HHS 1R01CA140458NCI NIH HHS R01 CA140458NCI NIH HHS T32 CA009135NIGMS NIH HHS T32 GM008688
6 · The paper itself

Abstract

Mitotic defects leading to aneuploidy have been recognized as a hallmark of tumor cells for over 100 years. Current data indicate that ∼85% of human cancers have missegregated chromosomes to become aneuploid. Some maintain a stable aneuploid karyotype, while others consistently missegregate chromosomes over multiple divisions due to chromosomal instability (CIN). Both aneuploidy and CIN serve as markers of poor prognosis in diverse human cancers. Despite this, aneuploidy is generally incompatible with viability during development, and some aneuploid karyotypes cause a proliferative disadvantage in somatic cells. In vivo, the intentional introduction of aneuploidy can promote tumors, suppress them, or do neither. Here, we summarize current knowledge of the effects of aneuploidy and CIN on proliferation and cell death in nontransformed cells, as well as on tumor promotion, suppression, and prognosis.

Indexed as

AneuploidyChromosomal InstabilityPolyploidyAnimalsCell Transformation, NeoplasticHumansNeoplasms

Identifiers

PMID23416057
PMCPMC3736819

What OpenQuestion holds

Textmetadata
LicenceTDM
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.