Naji Nour Sabiha, Sathish Mrudula, Karantanos Theodoros
Department of Oncology, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.
Department of Pediatrics, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Cancers (Basel). 2024 Nov 27;16(23):3974. doi: 10.3390/cancers16233974.
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，炎症信号参与其发病机制。细胞因子对AML的进展具有强大影响，并影响生存结果。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，降低生存率并导致耐药性。促炎介质如IL-11β、TNF-α和IL-6相对于抗炎介质如TGF-β和IL-10的优势与肿瘤进展有关。此外，炎性细胞因子有利于某些具有克隆性造血基因突变的造血干细胞和祖细胞群体。本文总结了目前关于AML中炎性细胞因子和信号通路的知识、它们的作用模式以及对免疫耐受和克隆性造血的影响，旨在寻找潜在的治疗干预措施以改善AML患者的临床结局。
