Humanitas Clinical and Research Center ; Rozzano, Italy ; Department of Medical Biotechnologies and Translational Medicine; Università degli Studi di Milano ; Rozzano, Italy.
Humanitas Clinical and Research Center ; Rozzano, Italy.
Oncoimmunology. 2015 Jan 7;3(12):e955337. doi: 10.4161/21624011.2014.955337. eCollection 2014 Dec.
Inflammatory chemokines are instrumental players in cancer-related inflammation contributing to numerous steps during tumor progression. In Kaposi's sarcoma, we have found that downregulation of the atypical chemokine receptor 2 (ACKR2) by the KRAS/BRAF/ERK pathway profoundly affects the tumor microenvironment, unleashing accumulation of tumor-associated macrophages that sustains tumor growth. This discovery extends our understanding on the role of inflammatory chemokines in tumor biology and provides rationale for their therapeutic targeting.
炎症趋化因子是癌症相关炎症中的重要参与者，有助于肿瘤进展的多个步骤。在卡波西肉瘤中，我们发现，KRAS/BRAF/ERK 通路下调非典型趋化因子受体 2 (ACKR2) ，会深刻影响肿瘤微环境，释放肿瘤相关巨噬细胞的积累，从而维持肿瘤生长。这一发现扩展了我们对炎症趋化因子在肿瘤生物学中的作用的理解，并为针对它们的治疗提供了依据。
