Evidence map›Paper›PMID 19258501›Full record

ArticleCancer research2009

Activation of meiosis-specific genes is associated with depolyploidization of human tumor cells following radiation-induced mitotic catastrophe.

Fiorenza Ianzini, Elizabeth A Kosmacek, Elke S Nelson, Eleonora Napoli, Jekaterina Erenpreisa, Martins Kalejs, Michael A Mackey

Abstract read
In one paragraph

Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 1 pooled it
–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

76 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Identification of a master regulator Msd1 that governs meiotic entry in a global basidiomycete pathogen.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Meiosis-specific genes play roles in ploidy reduction inProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Review
  6. Review
  7. Article
  8. Meiosis-specific genes play roles in ploidy reduction inbioRxiv : the preprint server for biology · 2025
    Article
  9. Surviving the Storm: The Role of Poly- and Depolyploidization in Tissues and Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Polyploidy as an Adaptation against Loss of Heterozygosity in Cancer.International journal of molecular sciences · 2022
    Article
  19. Review
  20. Review

16 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

7 authors.

Fiorenza IanziniDepartment of Pathology, University of Iowa, Seamans Center, University of Iowa, Iowa City, Iowa, USA. fiorenza-ianzini@uiowa.edu
Elizabeth A Kosmacek
Elke S Nelson
Eleonora Napoli
Jekaterina Erenpreisa
Martins Kalejs
Michael A Mackey

Funding

Viral VectorP30CA086862 · NCI · UNIVERSITY OF IOWA · PI Mark E Burkard · 2000 to 2026
$70.0M
LARGE SCALE DIGITAL CELL ANALYSIS SYSTEMR33CA094801 · NCI · UNIVERSITY OF IOWA · PI MACKEY, MICHAEL A · 2002 to 2004
$1.3M
NCI NIH HHS CA86862NCI NIH HHS CA/GM94801NCI NIH HHS P30 CA086862
6 · The paper itself

Abstract

Cancer is frequently characterized histologically by the appearance of large cells that are either aneuploid or polyploid. Aneuploidy and polyploidy are hallmarks of radiation-induced mitotic catastrophe (MC), a common phenomenon occurring in tumor cells with impaired p53 function following exposure to various cytotoxic and genotoxic agents. MC is characterized by altered expression of mitotic regulators, untimely and abnormal cell division, delayed DNA damage, and changes in morphology. We report here that cells undergoing radiation-induced MC are more plastic with regards to ploidy and that this plasticity allows them to reorganize their genetic material through reduction division to produce smaller cells which are morphologically indistinguishable from control cells. Experiments conducted with the large-scale digital cell analysis system are discussed and show that a small fraction of polyploid cancer cells formed via radiation-induced MC can survive and start a process of depolyploidization that yields various outcomes. Although most multipolar divisions failed and cell fusion occurred, some of these divisions were successful and originated a variety of cell progeny characterized by different ploidy. Among these ploidy phenotypes, a progeny of small mononucleated cells, indistinguishable from the untreated control cells, is often seen. We report here evidence that meiosis-specific genes are expressed in the polyploid cells during depolyploidization. Tumor cells might take advantage of the temporary change from a promitotic to a promeiotic division regimen to facilitate depolyploidization and restore the proliferative state of the tumor cell population. These events might be mechanisms by which tumor progression and resistance to treatment occur in vivo.

Indexed as

PolyploidyCell Cycle ProteinsCell NucleusChromosome SegregationDNA-Binding ProteinsGene Expression Regulation, NeoplasticHCT116 CellsHeLa CellsHumansMeiosisMetaphaseMitosisNeoplasmsCell Cycle ProteinsDMC1 protein, humanDNA-Binding Proteins

Identifiers

PMID19258501
PMCPMC2657811

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Registered trials

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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.