Evidence map›Paper›PMID 28633018›Full record

ArticleDevelopmental cell2017

Chromosome Mis-segregation Generates Cell-Cycle-Arrested Cells with Complex Karyotypes that Are Eliminated by the Immune System.

Stefano Santaguida, Amelia Richardson, Divya Ramalingam Iyer, Ons M'Saad, Lauren Zasadil, Kristin A Knouse, Yao Liang Wong, Nicholas Rhind, Arshad Desai, Angelika Amon

Abstract read
In one paragraph

Article in Developmental cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 228 papers.

0numbers the graph read from it
0cells of the map it votes in
228citing 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

228 citing papers in PubMed.

  1. Trial
  2. Review
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  13. PARP1 Suppression Drives ROS Resistance in Aneuploid Cancer Cells.bioRxiv : the preprint server for biology · 2026
    Article
  14. Cell confinement initiates a delayed but heritable loss of chromosomes.bioRxiv : the preprint server for biology · 2026
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Stefano SantaguidaDepartment of Biology, Koch Institute for Integrative Cancer Research at MIT, Howard Hughes Medical Institute, Massachusetts Institute of Technology, 76-543, Cambridge, MA 02138, USA. Electronic address: ste@mit.edu.
Amelia RichardsonDepartment of Cellular and Molecular Medicine, Ludwig Institute for Cancer Research, University of California, San Diego, La Jolla, CA 92093, USA.
Divya Ramalingam IyerDepartment of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA.
Ons M'SaadDepartment of Biology, Koch Institute for Integrative Cancer Research at MIT, Howard Hughes Medical Institute, Massachusetts Institute of Technology, 76-543, Cambridge, MA 02138, USA.
Lauren ZasadilDepartment of Biology, Koch Institute for Integrative Cancer Research at MIT, Howard Hughes Medical Institute, Massachusetts Institute of Technology, 76-543, Cambridge, MA 02138, USA.
Kristin A KnouseDepartment of Biology, Koch Institute for Integrative Cancer Research at MIT, Howard Hughes Medical Institute, Massachusetts Institute of Technology, 76-543, Cambridge, MA 02138, USA; Division of Health Sciences and Technology, Harvard Medical School, Boston, MA 02115, USA.
Yao Liang WongDepartment of Cellular and Molecular Medicine, Ludwig Institute for Cancer Research, University of California, San Diego, La Jolla, CA 92093, USA.
Nicholas RhindDepartment of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA.
Arshad DesaiDepartment of Cellular and Molecular Medicine, Ludwig Institute for Cancer Research, University of California, San Diego, La Jolla, CA 92093, USA.
Angelika AmonDepartment of Biology, Koch Institute for Integrative Cancer Research at MIT, Howard Hughes Medical Institute, Massachusetts Institute of Technology, 76-543, Cambridge, MA 02138, USA. Electronic address: angelika@mit.edu.

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
Medical Scientist Training ProgramT32GM007753 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WALENSKY, LOREN DAVID · 1985 to 2021
$50.0M
Kinetochore Specification and FunctionR01GM074215 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DESAI, ARSHAD · 2005 to 2025
$8.2M
Predoctoral and Postdoctoral Training in Cancer Cell BiologyT32CA067754 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JEAN Y.J. WANG · 1995 to 2026
$6.5M
REGULATION OF THE MEIOTIC CELL CYCLER01GM062207 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI AMON, ANGELIKA B · 2001 to 2016
$3.8M
Regulation of Mitosis by Proteolysis in YeastR01GM056800 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI AMON, ANGELIKA B · 2004 to 2015
$3.4M
Causes and consequences of aneuploidyR35GM118066 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI AMON, ANGELIKA B · 2016 to 2020
$1.9M
Mitotic exit controlR01HD085866 · NICHD · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI AMON, ANGELIKA B · 2015 to 2019
$1.6M
Regulation of mitosis by proteolysis in yeastR01CA206157 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI AMON, ANGELIKA B · 2016 to 2020
$1.4M
The Regulation of DNA Replication KineticsR01GM098815 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI RHIND, NICHOLAS R · 2012 to 2015
$1.3M
Howard Hughes Medical InstituteNCI NIH HHS P30 CA014051NCI NIH HHS R01 CA206157NCI NIH HHS T32 CA067754NICHD NIH HHS R01 HD085866NIGMS NIH HHS R01 GM056800NIGMS NIH HHS R01 GM062207NIGMS NIH HHS R01 GM074215NIGMS NIH HHS R01 GM098815NIGMS NIH HHS R35 GM118066NIGMS NIH HHS T32 GM007753
6 · The paper itself

Abstract

Aneuploidy, a state of karyotype imbalance, is a hallmark of cancer. Changes in chromosome copy number have been proposed to drive disease by modulating the dosage of cancer driver genes and by promoting cancer genome evolution. Given the potential of cells with abnormal karyotypes to become cancerous, do pathways that limit the prevalence of such cells exist? By investigating the immediate consequences of aneuploidy on cell physiology, we identified mechanisms that eliminate aneuploid cells. We find that chromosome mis-segregation leads to further genomic instability that ultimately causes cell-cycle arrest. We further show that cells with complex karyotypes exhibit features of senescence and produce pro-inflammatory signals that promote their clearance by the immune system. We propose that cells with abnormal karyotypes generate a signal for their own elimination that may serve as a means for cancer cell immunosurveillance.

Indexed as

AneuploidyChromosome AberrationsCell Cycle CheckpointsChromosomal InstabilityChromosome SegregationGene DosageGenomic InstabilityHumansKaryotypeNeoplasmsaneuploidycancergenome instabilityimmune systemsenescence

Identifiers

PMID28633018
PMCPMC5536848

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.