作者
Laura Senovilla,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 María Fimia,Mauro Piacentini,Antonio Fueyo,Nicole L. Messina,Ming Li,Christopher J. Chan,Verena Sigl,Guillaume Pourcher,Christoph Ruckenstuhl,Didac Carmona‐Gutiérrez,Vladimir Lazar,Josef Penninger,Frank Madeo,Carlos López-Otı́n,Mark J. Smyth,Laurence Zitvogel,Maria Castedo,Guido Kroemer
摘要
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.