Muto Tomoya
Division of Cancer RNA Research, National Cancer Center Research Institute.
Rinsho Ketsueki. 2023;64(9):962-969. doi: 10.11406/rinketsu.64.962.
Myeloid malignancies are composed of multiple clonal hematopoietic disorders, including myelodysplastic syndrome, myeloproliferative neoplasms, and acute myeloid leukemia. Inflammation is already known to play an important role in the pathogenesis of an extensive variety of malignancies, and its significance in myeloid malignancies is becoming more widely recognized. Specifically, cell-intrinsic and -extrinsic activation of the innate immune signaling pathway, as well as elevation of proinflammatory cytokines via innate immune signaling downstream signaling, have been demonstrated. Furthermore, the inflammatory microenvironment refers to the bone marrow environment rich in inflammatory signaling molecules that surround hematopoietic malignant cells, and its role in the pathogenesis of myeloid malignancies has been extensively studied in recent years. Herein, we present the latest findings and discuss how innate immune signaling activation and the inflammatory bone marrow microenvironment contribute to the pathogenesis of myeloid malignancies.
髓系恶性肿瘤由多种克隆性造血疾病组成,包括骨髓增生异常综合征、骨髓增殖性肿瘤和急性髓系白血病。炎症在多种恶性肿瘤的发病机制中已被证实发挥重要作用,其在髓系恶性肿瘤中的重要性也越来越受到广泛认可。具体而言,已证实先天性免疫信号通路的细胞内源性和外源性激活,以及通过先天性免疫信号下游信号传导导致促炎细胞因子水平升高。此外,炎症微环境是指富含炎症信号分子的骨髓环境,其围绕造血恶性细胞,近年来对其在髓系恶性肿瘤发病机制中的作用进行了广泛研究。在此,我们介绍最新研究结果,并讨论先天性免疫信号激活和炎症性骨髓微环境如何促进髓系恶性肿瘤的发病机制。