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©2019 American Association for Cancer Research.Technologies and Products Specialist for Mid-Atlantic Macintosh User Groups Team (what's it do?):īroadcast any audio from your Mac over the internet or LAN Our data have identified the classical complement pathway as a key inflammatory mechanism activated by the cooperation between tumor cells and TAMs, favoring cancer progression, and highlight potential therapeutic targets to restore an efficient immune reaction to cancer. However, the ccRCC tumors infiltrated with high densities of C1q-producing TAMs exhibited an immunosuppressed microenvironment, characterized by high expression of immune checkpoints (i.e., PD-1, Lag-3, PD-L1, and PD-L2). Accordingly, mice deficient in C1q, C4, or C3 displayed decreased tumor growth. The in situ orchestrated production of C1q by tumor-associated macrophages (TAM) and C1r, C1s, C4, and C3 by tumor cells associated with IgG deposits, led to C1 complex assembly, and complement activation. High densities of cells producing classical complement pathway components C1q and C4 and the presence of C4 activation fragment deposits in primary tumors correlated with poor prognosis. To understand how the complement cascade is activated in ccRCC and impacts patients' clinical outcome, primary tumors from three patient cohorts ( n = 106, 154, and 43), ccRCC cell lines, and tumor models in complement-deficient mice were used. By data mining, we identified ccRCC as a cancer type expressing concomitantly high expression of the components that are part of the classical complement pathway. However, the activation pathways that generate C5a in tumors remain obscure. Complement is a key factor in tissue inflammation, favoring cancer progression through the production of complement component 5a (C5a). renal cell carcinoma (ccRCC) possesses an unmet medical need, particularly at the metastatic stage, when surgery is ineffective. 15 Sorbonne Paris Cite, Cordeliers Research Center, University Paris Descartes Paris 5, Paris, France.2 Sorbonne Paris Cite, Cordeliers Research Center, University Paris Descartes Paris 5, Paris, France. 1 INSERM, UMR_S 1138, Cordeliers Research Center, Team "Complement and diseases", Paris, France. 14 Department of Urology, Georges Pompidou European Hospital, Assistance Publique Hopitaux de Paris, Paris, France.13 Department of Medicine, Imperial College London, London, United Kingdom.12 Pierre Fabre Research Institute, Toulouse, France.11 Department of Pathology, Institut Mutualiste Montsouris, Paris, France.10 Department of Pathology, Georges Pompidou European Hospital, Assistance Publique Hopitaux de Paris, Paris, France.9 Department of Pathology, Institut Universitaire du Cancer Toulouse - Oncopole, Toulouse, France.8 Department of Urology, Institut Mutualiste Montsouris, Paris, France.7 Department of Oncology, Georges Pompidou European Hospital, Assistance Publique Hopitaux de Paris, Paris, France.6 Programme Cartes d'Identité des Tumeurs, Ligue Nationale contre le Cancer, Paris, France.5 INSERM, UMR_S 1138, Cordeliers Research Center, Team "Cancer, Immune Control and Escape", Paris, France.4 INSERM, UMR_S 1138, Cordeliers Research Center, Team "Complement and diseases", Paris, France.3 Cordeliers Research Center, Sorbonne University, Paris, France.1 INSERM, UMR_S 1138, Cordeliers Research Center, Team "Complement and diseases", Paris, France.
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