An Immunosurveillance Mechanism Controls Cancer Cell Ploidy-Reference-Cited by-同舟云学术

An Immunosurveillance Mechanism Controls Cancer Cell Ploidy

Published:2012-09-28 Issue:6102 Volume:337 Page:1678-1684
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Senovilla Laura¹²³,Vitale Ilio¹²³,Martins Isabelle¹²³,Tailler Maximilien¹²³,Pailleret Claire¹²³,Michaud Mickaël¹²³,Galluzzi Lorenzo¹²³,Adjemian Sandy¹²³,Kepp Oliver¹²³,Niso-Santano Mireia¹²³,Shen Shensi¹²³,Mariño Guillermo¹²³,Criollo Alfredo¹²³,Boilève Alice¹²³,Job Bastien²⁴⁵,Ladoire Sylvain⁶⁷,Ghiringhelli François⁶⁷,Sistigu Antonella²³⁸,Yamazaki Takahiro²³⁸,Rello-Varona Santiago¹²³,Locher Clara²³⁸,Poirier-Colame Vichnou²³⁸,Talbot Monique²,Valent Alexander⁹,Berardinelli Francesco¹⁰,Antoccia Antonio¹⁰,Ciccosanti Fabiola¹¹,Fimia Gian Maria¹¹,Piacentini Mauro¹¹¹²,Fueyo Antonio¹³,Messina Nicole L.¹⁴¹⁵,Li Ming¹⁴,Chan Christopher J.¹⁴¹⁶,Sigl Verena¹⁷,Pourcher Guillaume³¹⁸¹⁹,Ruckenstuhl Christoph²⁰,Carmona-Gutierrez Didac²⁰,Lazar Vladimir²⁴⁵,Penninger Josef M.¹⁷,Madeo Frank²⁰,López-Otín Carlos²¹,Smyth Mark J.¹⁴¹⁶,Zitvogel Laurence²³⁸²²,Castedo Maria¹²³,Kroemer Guido¹²³²⁴²⁵²⁶

Affiliation:

1. INSERM, U848, Villejuif, France.

2. Institut Gustave Roussy, Villejuif, France.

3. Université Paris Sud/Paris 11, Faculté de Médecine, Le Kremlin Bicêtre, France.

4. Unité de Génomique Fonctionnelle et Bioinformatique, Villejuif, France.

5. Genomique Platform, Villejuif, France.

6. Department of Medical Oncology, Georges François Leclerc Center, Dijon, France.

7. Institut National de la Santé et de la Recherche Médicale, Avenir Team INSERM, CRI-866 University of Burgundy, Dijon, France.

8. INSERM, U1015, Villejuif, France.

9. Pathologie Moléculaire, Departement De Biologie et Pathologie Médicales, Villejuif, France.

10. Dipartimento Di Biologia, Università Roma Tre, Rome, Italy.

11. National Institute for Infectious Diseases L. Spallanzani, Rome, Italy.

12. Department of Biology, University of Rome “Tor Vergata,” Rome, Italy.

13. Departamento de Biología Funcional, Facultad de Medicina, Instituto Universitario de Oncología (IUOPA), Universidad de Oviedo, Oviedo, Spain.

14. Cancer Immunology Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia.

15. Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, Victoria, Australia.

16. Department of Immunology, Monash University, Prahran, Victoria, Australia.

17. Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna, Austria.

18. Department of Minimal Invasive Surgery, Antoine Béclère Hospital, AP-HP, Clamart, France.

19. INSERM, U972, Le Kremlin Bicêtre, France.

20. Institute for Molecular Bioscience, Graz, Austria.

21. Departamento de Bioquímica y Biología Molecular, Facultad de Medicina, IUOPA, Universidad de Oviedo, Oviedo, Spain.

22. Center of Clinical Investigations in Biotherapies of Cancer (CICBT) 507, Villejuif, France.

23. Metabolomics Platform, Institut Gustave Roussy, Villejuif, France.

24. Centre de Recherche des Cordeliers, Paris, France.

25. Pôle de Biologie, Hôpital Européen Georges Pompidou, Assistance Publique–Hôpitaux de Paris (AP-HP), Paris, France.

26. Université Paris Descartes/Paris 5, Sorbonne Paris Cité, Paris, France.

Abstract

Keeping Cancer Cells At Bay Cancer cells are often aneuploid; that is, they have an abnormal number of chromosomes. But to what extent this contributes to the tumorigenic phenotype is not clear. Senovilla et al. (p. 1678 ; see the Perspective by

Zanetti and Mahadevan

) found that tetraploidization of cancer cells can cause them to become immunogenic and thus aid in their clearance from the body by the immune system. Cells with excess chromosomes put stress on the endoplasmic reticulum, which leads to movement of the protein calreticulin to the cell surface. Calreticulin exposure in turn caused recognition of cancer cells in mice by the host immune system. Thus, the immune system appears to serve a protective role in eliminating hyperploid cells that must be overcome to allow unrestricted growth of cancer cells.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference50 articles.

1. Intrinsic tumour suppression

2. An Oncogene-Induced DNA Damage Model for Cancer Development

3. Oncogenic stress sensed by the immune system: role of natural killer cell receptors

4. Death and anti-death: tumour resistance to apoptosis

5. Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas

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