癌症研究
医学
肿瘤坏死因子α
巨细胞瘤
受体
调节器
染色体易位
病理
巨噬细胞
细胞
信号转导
转录因子
髓系细胞
电池类型
生物
滑膜
关节炎
髓样
促炎细胞因子
免疫学
靶向治疗
炎症
生物信息学
骨巨细胞瘤
肿瘤坏死因子受体
病理生理学
渗透(HVAC)
巨噬细胞集落刺激因子
巨细胞
基因表达调控
作者
P. Humbert,Charlotte Vialle,Marie Chevalerias,Vincent Crenn,Denis Waast,Marie‐Astrid Boutet,Frédéric Blanchard,Benoît Le Goff
标识
DOI:10.1016/j.cytogfr.2025.10.007
摘要
Diffuse and Localized Tenosynovial Giant Cell Tumors (D-/L-TGCT) are two closely related forms of benign tumors of the joint characterized by uncontrolled macrophage infiltration and proliferation. Both forms arise from similar translocation events in synovial fibroblasts involving the Colony Stimulating Factor 1 (CSF1) gene, the major regulator of myeloid cell survival and activity. This review first describes CSF1 gene structure and protein expression as well as signaling through its receptor (CSF1R). Then, genetic alterations observed in TGCT patients are described in depth. The main features are translocations that remove the 3' regulatory elements of CSF1 messenger RNA, driving its overexpression and the abnormal recruitment of non neoplastic macrophages leading to tumor growth. This review then focuses on the resulting histopathological features characterizing the disease, as well as the available treatments targeting the CSF1 axis. Systemic therapies targeting CSF1 or its receptor are valuable for relapsing or inoperable cases, especially D-TGCT, but their use is still limited by heavy side effects and unresponsive tumors. Overall, our understanding of the pathophysiology of these tumors, the efficacy and limitations of current therapeutic options, and the questions that remain unanswered open new avenues for research and provide opportunities to further improve patient care.
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