Research Perspectives:

Autophagy-dependent danger signaling and adaptive immunity to poorly immunogenic tumors

Guido Kroemer and Lorenzo Galluzzi _

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Oncotarget. 2017; 8:5686-5691. https://doi.org/10.18632/oncotarget.13892

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Guido Kroemer1,2,3,4,5,6,7 and Lorenzo Galluzzi1,2,3,4,8,9

1 Equipe 11 Labellisée par la Ligue Contre le Cancer, Centre de Recherche des Cordeliers, Paris, France

2 INSERM, U1138, Paris, France

3 Université Paris Descartes/Paris V, Sorbonne Paris Cité, Paris, France

4 Université Pierre et Marie Curie/Paris VI, Paris, France

5 Metabolomics and Cell Biology Platforms, Gustave Roussy Comprehensive Cancer Institute, Villejuif, France

6 Pôle de Biologie, Hopitâl Européen George Pompidou, AP-HP, Paris, France

7 Department of Women’s and Children’s Health, Karolinska University Hospital, Stockholm, Sweden

8 Gustave Roussy Comprehensive Cancer Institute, Villejuif, France

9 Department of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA

Correspondence to:

Lorenzo Galluzzi, email:

Keywords: ATP; chloroquine; damage-associated molecular patterns; doxorubicin; immunogenic cell death; radiation therapy

Received: October 27, 2016 Accepted: November 14, 2016 Published: December 10, 2016


Recent data suggest that autophagy does not influence spontaneous and therapy-elicited tumor infiltration by immune cells in murine models of melanoma and breast carcinoma. These findings, which have been obtained in the absence of a therapeutically relevant anticancer immune response, indicate that the intrinsically low immunogenicity of some tumors cannot be compensated for by increased danger signaling.

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