Evidence map›Paper›PMID 23019653›Full record

ArticleScience (New York, N.Y.)2012

An immunosurveillance mechanism controls cancer cell ploidy.

Laura Senovilla, Ilio Vitale, Isabelle Martins, Maximilien Tailler, Claire Pailleret, Mickaël Michaud, Lorenzo Galluzzi, Sandy Adjemian, Oliver Kepp, Mireia Niso-Santano and 35 more

Abstract read
PubMed Publisher
In one paragraph

Article in Science (New York, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 270 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
270citing 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

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

  1. Pooled it
  2. Trial
  3. Review
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  5. Article
  6. Article
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  12. 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
  13. Article
  14. Article
  15. Review
  16. Article
  17. Chemotherapy Drives Tertiary Lymphoid Structures That Correlate with ICI-Responsive TCF1+CD8+ T Cells in Metastatic Ovarian Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  18. Impact of Areca Catechu Kombucha on Inflammatory Markers and Gut Microbiota - a Review.Medical archives (Sarajevo, Bosnia and Herzegovina) · 2025
    Review
  19. Review
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

45 authors.

Laura SenovillaINSERM, U848, Villejuif, France.
Ilio Vitale
Isabelle Martins
Maximilien Tailler
Claire Pailleret
Mickaël Michaud
Lorenzo Galluzzi
Sandy Adjemian
Oliver Kepp
Mireia Niso-Santano
Shensi Shen
Guillermo Mariño
Alfredo Criollo
Alice Boilève
Bastien Job
Sylvain Ladoire
François Ghiringhelli
Antonella Sistigu
Takahiro Yamazaki
Santiago Rello-Varona
Clara Locher
Vichnou Poirier-Colame
Monique Talbot
Alexander Valent
Francesco Berardinelli
Antonio Antoccia
Fabiola Ciccosanti
Gian Maria Fimia
Mauro Piacentini
Antonio Fueyo
Nicole L Messina
Ming Li
Christopher J Chan
Verena Sigl
Guillaume Pourcher
Christoph Ruckenstuhl
Didac Carmona-Gutierrez
Vladimir Lazar
Josef M Penninger
Frank Madeo
Carlos López-Otín
Mark J Smyth
Laurence Zitvogel
Maria Castedo
Guido Kroemer

Funding

Austrian Science Fund FWF P 23490Austrian Science Fund FWF P 24381Austrian Science Fund FWF W 1226
6 · The paper itself

Abstract

Cancer cells accommodate multiple genetic and epigenetic alterations that initially activate intrinsic (cell-autonomous) and extrinsic (immune-mediated) oncosuppressive mechanisms. Only once these barriers to oncogenesis have been overcome can malignant growth proceed unrestrained. Tetraploidization can contribute to oncogenesis because hyperploid cells are genomically unstable. We report that hyperploid cancer cells become immunogenic because of a constitutive endoplasmic reticulum stress response resulting in the aberrant cell surface exposure of calreticulin. Hyperploid, calreticulin-exposing cancer cells readily proliferated in immunodeficient mice and conserved their increased DNA content. In contrast, hyperploid cells injected into immunocompetent mice generated tumors only after a delay, and such tumors exhibited reduced DNA content, endoplasmic reticulum stress, and calreticulin exposure. Our results unveil an immunosurveillance system that imposes immunoselection against hyperploidy in carcinogen- and oncogene-induced cancers.

Indexed as

Immunologic SurveillancePloidiesAnimalsCalreticulinCell Line, TumorCommon Variable ImmunodeficiencyDNA, NeoplasmEndoplasmic Reticulum StressEukaryotic Initiation Factor-2HumansImmunocompetenceMiceMice, Inbred BALB CNeoplasmsPhosphorylationCalreticulinDNA, NeoplasmEukaryotic Initiation Factor-2

Identifiers

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.