Autophagy-dependent anticancer immune responses induced by chemotherapeutic agents in mice.

@article{Michaud2011AutophagydependentAI,
  title={Autophagy-dependent anticancer immune responses induced by chemotherapeutic agents in mice.},
  author={Mick{\"a}el Michaud and Isabelle Christine V. S. Martins and Abdul Qader Sukkurwala and Sandy Adjemian and Yuting Ma and Patrizia Pellegatti and Shensi Shen and Oliver Kepp and Marie Scoazec and Gr{\'e}goire Mignot and Santiago Rello-Varona and Maximilien Tailler and Laurie Menger and Erika Vacchelli and Lorenzo Galluzzi and François Ghiringhelli and Francesco Di Virgilio and Laurence Zitvogel and Guido Kroemer},
  journal={Science},
  year={2011},
  volume={334 6062},
  pages={1573-7}
}
Antineoplastic chemotherapies are particularly efficient when they elicit immunogenic cell death, thus provoking an anticancer immune response. Here we demonstrate that autophagy, which is often disabled in cancer, is dispensable for chemotherapy-induced cell death but required for its immunogenicity. In response to chemotherapy, autophagy-competent, but not autophagy-deficient, cancers attracted dendritic cells and T lymphocytes into the tumor bed. Suppression of autophagy inhibited the… CONTINUE READING
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Thus , autophagy is essential for the immunogenic release of ATP from dying cells , and increased extracellular ATP concentrations improve the efficacy of antineoplastic chemotherapies when autophagy is disabled .
Antineoplastic chemotherapies are particularly efficient when they elicit immunogenic cell death , thus provoking an anticancer immune response .
Here we demonstrate that autophagy , which is often disabled in cancer , is dispensable for chemotherapy - induced cell death but required for its immunogenicity .
Here we demonstrate that autophagy , which is often disabled in cancer , is dispensable for chemotherapy - induced cell death but required for its immunogenicity .
Here we demonstrate that autophagy , which is often disabled in cancer , is dispensable for chemotherapy - induced cell death but required for its immunogenicity .
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