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Liu, Peng; Zhao, Liwei; Pol, Jonathan; Levesque, Sarah; Petrazzuolo, Adriana; Pfirschke, Christina; Engblom, Camilla; Rickelt, Steffen; Yamazaki, Takahiro; Iribarren, Kristina; Senovilla, Laura; Bezu, Lucillia; Vacchelli, Erika; Sica, Valentina; Melis, Andréa; Martin, Tiffany; Xia, Lin; Yang, Heng; Li, Qingqing; Chen, Jinfeng; Durand, Sylvère; Aprahamian, Fanny; Lefevre, Deborah; Broutin, Sophie; Paci, Angelo; Bongers, Amaury; Minard-Colin, Veronique; Tartour, Eric; Zitvogel, Laurence; Apetoh, Lionel; Ma, Yuting; Pittet, Mikael J; Kepp, Oliver; Kroemer, Guido
Nature communications, 04/2019, Volume: 10, Issue: 1Journal Article
Immunogenic cell death (ICD) converts dying cancer cells into a therapeutic vaccine and stimulates antitumor immune responses. Here we unravel the results of an unbiased screen identifying high-dose (10 µM) crizotinib as an ICD-inducing tyrosine kinase inhibitor that has exceptional antineoplastic activity when combined with non-ICD inducing chemotherapeutics like cisplatin. The combination of cisplatin and high-dose crizotinib induces ICD in non-small cell lung carcinoma (NSCLC) cells and effectively controls the growth of distinct (transplantable, carcinogen- or oncogene induced) orthotopic NSCLC models. These anticancer effects are linked to increased T lymphocyte infiltration and are abolished by T cell depletion or interferon-γ neutralization. Crizotinib plus cisplatin leads to an increase in the expression of PD-1 and PD-L1 in tumors, coupled to a strong sensitization of NSCLC to immunotherapy with PD-1 antibodies. Hence, a sequential combination treatment consisting in conventional chemotherapy together with crizotinib, followed by immune checkpoint blockade may be active against NSCLC.
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