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Restricting Glycolysis Preserves T Cell Effector Functions and Augments Checkpoint Therapy

URN to cite this document:
urn:nbn:de:bvb:355-epub-408127
Renner, Kathrin ; Bruss, Christina ; Schnell, Annette ; Koehl, Gudrun ; Becker, Holger M. ; Fante, Matthias ; Menevse, Ayse-Nur ; Kauer, Nathalie ; Blazquez, Raquel ; Hacker, Lisa ; Decking, Sonja-Maria ; Bohn, Toszka ; Faerber, Stephanie ; Evert, Katja ; Aigle, Lisa ; Amslinger, Sabine ; Landa, Maria ; Krijgsman, Oscar ; Rozeman, Elisa A. ; Brummer, Christina ; Siska, Peter J. ; Singer, Katrin ; Pektor, Stefanie ; Miederer, Matthias ; Peter, Katrin ; Gottfried, Eva ; Herr, Wolfgang ; Marchiq, Ibtisam ; Pouyssegur, Jacques ; Roush, William R. ; Ong, SuFey ; Warren, Sarah ; Pukrop, Tobias ; Beckhove, Philipp ; Lang, Sven A. ; Bopp, Tobias ; Blank, Christian U. ; Cleveland, John L. ; Oefner, Peter J. ; Dettmer, Katja ; Selby, Mark ; Kreutz, Marina
Date of publication of this fulltext: 10 Oct 2019 14:34


Abstract

Tumor-derived lactic acid inhibits T and natural killer (NK) cell function and, thereby, tumor immunosurveillance. Here, we report that melanoma patients with high expression of glycolysis-related genes show a worse progression free survival upon anti-PD1 treatment. The non-steroidal anti-inflammatory drug (NSAID) diclofenac lowers lactate secretion of tumor cells and improves anti-PD1-induced T ...

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