Acute myeloid leukemia (AML) is an aggressive hematologic malignancy, and inflammatory signaling is involved in its pathogenesis. Cytokines exert a robust effect on the progression of AML and affect survival outcomes. The dysregulation in the cytokine network may foster a pro-tumorigenic microenvironment, increasing leukemic cell proliferation, decreasing survival and driving drug resistance. The dominance of pro-inflammatory mediators such as IL-11β, TNF-α and IL-6 over anti-inflammatory mediators such as TGF-β and IL-10 has been implicated in tumor progression. Additionally, inflammatory cytokines have favored certain populations of hematopoietic stem and progenitor cells with mutated clonal hematopoiesis genes. This article summarizes current knowledge about inflammatory cytokines and signaling pathways in AML, their modes of action and the implications for immune tolerance and clonal hematopoiesis, with the aim of finding potential therapeutic interventions to improve clinical outcomes in AML patients.
急性髓系白血病（AML）是一种侵袭性血液系统恶性肿瘤，其发病机制涉及炎症信号传导。细胞因子对AML的进展具有显著影响，并影响患者的生存结局。细胞因子网络的失调可能促进促肿瘤微环境的形成，增加白血病细胞增殖、降低生存率并驱动耐药性。促炎介质（如IL-1β、TNF-α和IL-6）相对于抗炎介质（如TGF-β和IL-10）的优势地位与肿瘤进展密切相关。此外，炎症细胞因子倾向于支持携带克隆造血基因突变的特定造血干细胞和祖细胞群体。本文综述了当前关于AML中炎症细胞因子及其信号通路的研究进展，包括其作用模式以及对免疫耐受和克隆造血的影响，旨在寻找潜在的治疗干预措施以改善AML患者的临床结局。
Inflammation and Related Signaling Pathways in Acute Myeloid Leukemia
肿瘤(癌症)患者之家