Evidence map›Paper›PMID 25197064›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Chromosome instability induced by Mps1 and p53 mutation generates aggressive lymphomas exhibiting aneuploidy-induced stress.

Floris Foijer, Stephanie Z Xie, Judith E Simon, Petra L Bakker, Nathalie Conte, Stephanie H Davis, Eva Kregel, Jos Jonkers, Allan Bradley, Peter K Sorger

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

66 citing papers in PubMed, 109 citations in OpenAlex.

  1. Review
  2. Unraveling the Molecular Mechanisms Underlying Spontaneous Multipolar Mitosis Through CIN-seq.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Non-cell-autonomous mechanisms of tumor initiation and relapse by chromosomal instability.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. Article
  6. Article
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  8. Meiosis-specific genes play roles in ploidy reduction inbioRxiv : the preprint server for biology · 2025
    Article
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  11. Review
  12. Article
  13. Review
  14. Article
  15. The two sides of chromosomal instability: drivers and brakes in cancer.Signal transduction and targeted therapy · 2024
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

6 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

10 authors at 7 institutions in 3 countries.

Floris FoijerEuropean Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, NL-9713 AV, Groningen, The Netherlands; Department of Systems Biology, Harvard Medical School, Boston, MA 02115; Mouse Genomics, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, United Kingdom; and f.foijer@umcg.nl peter_sorger@hms.harvard.edu.
Stephanie Z XieDepartment of Systems Biology, Harvard Medical School, Boston, MA 02115;
Judith E SimonEuropean Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, NL-9713 AV, Groningen, The Netherlands;
Petra L BakkerEuropean Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, NL-9713 AV, Groningen, The Netherlands;
Nathalie ConteMouse Genomics, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, United Kingdom; and.
Stephanie H DavisDepartment of Systems Biology, Harvard Medical School, Boston, MA 02115;
Eva KregelDivision of Molecular Pathology, The Netherlands Cancer Institute, NL-1066 CX, Amsterdam, The Netherlands.
Jos JonkersDivision of Molecular Pathology, The Netherlands Cancer Institute, NL-1066 CX, Amsterdam, The Netherlands.
Allan BradleyMouse Genomics, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, United Kingdom; and.
Peter K SorgerDepartment of Systems Biology, Harvard Medical School, Boston, MA 02115; f.foijer@umcg.nl peter_sorger@hms.harvard.edu.
Center for Systems Biology · USWellcome Sanger Institute · GBHarvard University · USOncode Institute · NLThe Netherlands Cancer Institute · NLUniversity Medical Center Groningen · NLUniversity of Groningen · NL

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
Quantitative Analysis of Cell Death Pathways in CancerP01CA139980 · NCI · HARVARD MEDICAL SCHOOL · PI WEISSLEDER, MD, PHD, RALPH · 2010 to 2014
$9.0M
CELL AND TUMOR GENETICS OF MITOTIC ARREST CHECKPOINTSR01CA084179 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SORGER, PETER KARL · 2000 to 2010
$3.5M
NCI NIH HHS CA084179NCI NIH HHS CA139980NCI NIH HHS P01 CA139980NCI NIH HHS P30 CA014051NCI NIH HHS P30-CA14051NCI NIH HHS R01 CA084179Wellcome Trust
6 · The paper itself

Abstract

Aneuploidy is a hallmark of human solid cancers that arises from errors in mitosis and results in gain and loss of oncogenes and tumor suppressors. Aneuploidy poses a growth disadvantage for cells grown in vitro, suggesting that cancer cells adapt to this burden. To understand better the consequences of aneuploidy in a rapidly proliferating adult tissue, we engineered a mouse in which chromosome instability was selectively induced in T cells. A flanked by Lox mutation was introduced into the monopolar spindle 1 (Mps1) spindle-assembly checkpoint gene so that Cre-mediated recombination would create a truncated protein (Mps1(DK)) that retained the kinase domain but lacked the kinetochore-binding domain and thereby weakened the checkpoint. In a sensitized p53(+/-) background we observed that Mps1(DK/DK) mice suffered from rapid-onset acute lymphoblastic lymphoma. The tumors were highly aneuploid and exhibited a metabolic burden similar to that previously characterized in aneuploid yeast and cultured cells. The tumors nonetheless grew rapidly and were lethal within 3-4 mo after birth.

Indexed as

AneuploidyAnimalsChromosomal InstabilityChromosome AberrationsClone CellsGene DosageGene Expression Regulation, LeukemicHeterozygoteHumansKaryotypingMiceM Phase Cell Cycle CheckpointsMutationPrecursor T-Cell Lymphoblastic Leukemia-LymphomaProtein Serine-Threonine KinasesProtein Structure, TertiaryProtein Serine-Threonine KinasesTtk protein, mouseTumor Suppressor Protein p53chromosomal instabilityCINmouse modelsT-cell acute lymphoblastic lymphomatumor metabolism

Identifiers

PMID25197064
PMCPMC4169945
OpenAlexW2135509865

What OpenQuestion holds

Textmetadata
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.