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Aranda F, Chaba K, Bloy N, et al. Immune effectors responsible for the elimination of hyperploid cancer cells. Oncoimmunology. 2018;7(8):e1463947doi: 10.1080/2162402X.2018.1463947.
Aranda, F., Chaba, K., Bloy, N., Garcia, P., Bordenave, C., Martins, I., Stoll, G., Tesniere, A., Kroemer, G., & Senovilla, L. (2018). Immune effectors responsible for the elimination of hyperploid cancer cells. Oncoimmunology, 7(8), e1463947. https://doi.org/10.1080/2162402X.2018.1463947
Aranda, Fernando, et al. "Immune effectors responsible for the elimination of hyperploid cancer cells." Oncoimmunology vol. 7,8 (2018): e1463947. doi: https://doi.org/10.1080/2162402X.2018.1463947
Aranda F, Chaba K, Bloy N, Garcia P, Bordenave C, Martins I, Stoll G, Tesniere A, Kroemer G, Senovilla L. Immune effectors responsible for the elimination of hyperploid cancer cells. Oncoimmunology. 2018 May 21;7(8):e1463947. doi: 10.1080/2162402X.2018.1463947. eCollection 2018. PMID: 30221060; PMCID: PMC6136857.
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Oncoimmunology. 2018 May 21;7(8):e1463947. doi: 10.1080/2162402X.2018.1463947. eCollection 2018.

Immune effectors responsible for the elimination of hyperploid cancer cells.

Oncoimmunology

Fernando Aranda, Kariman Chaba, Norma Bloy, Pauline Garcia, Chloé Bordenave, Isabelle Martins, Gautier Stoll, Antoine Tesniere, Guido Kroemer, Laura Senovilla

Affiliations

  1. INSERM U1138-Equipe 11 labellisée Ligue contre le Cancer, Centre de Recherche des Cordeliers, Paris, France.
  2. Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
  3. Université Pierre et Marie Curie, Paris, France.
  4. Gustave Roussy Cancer Campus, Villejuif, France.
  5. Ilumens Simulation Department, Paris Descartes University, Paris, France.
  6. Surgical Intensive Care Department, Hôpital Européen Georges Pompidou, AP-HP, Paris, France.
  7. Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, Paris, France.
  8. Karolinska Institute, Department of Women's and Children's Health, Karolinska University Hospital, Stockholm, Sweden.

PMID: 30221060 PMCID: PMC6136857 DOI: 10.1080/2162402X.2018.1463947

Abstract

The immune system avoids oncogenesis and slows down tumor progression through a mechanism called immunosurveillance. Nevertheless, some malignant cells manage to escape from immune control and form clinically detectable tumors. Tetraploidy, which consists in the intrinsically unstable duplication of the genome, is considered as a (pre)-cancerous event that can result in aneuploidy and contribute to oncogenesis. We previously described the fact that tetraploid cells can be eliminated by the immune system. Here, we investigate the role of different innate and acquired immune effectors by inoculating hyperploid cancer cells into wild type or mice bearing different immunodeficient genotypes (

Keywords: cancer; genomic instability; hyperploidy; immunoselection; immunosurveillance

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