Uterine stromal-derived tumors encompass a spectrum of rare neoplasms, ranging from benign endometrial stromal nodules to aggressive high-grade endometrial stromal sarcomas and undifferentiated uterine sarcomas. The classification of these tumors has advanced through molecular and immunohistochemical profiling, but the role of the extracellular matrix (ECM) in their biology is only beginning to be understood. The ECM provides both structural support and dynamic signaling cues, regulating tumor cell proliferation, invasion, angiogenesis, and immune evasion. Altered expression of collagens, proteoglycans, glycosaminoglycans, and matricellular proteins reshapes stromal architecture and contributes to disease progression. Moreover, ECM remodeling enzymes such as matrix metalloproteinases, together with cross-linking factors, create a stiff and pro-tumorigenic microenvironment that facilitates invasion and therapeutic resistance. Furthermore, these matrix alterations intersect with angiogenesis, mechanotransduction pathways, and immune modulation. Studies to date describe the role of ECM molecules in the function of the physiological uterine tissue and data for the uterine stroma-derived tumors is scarce. This review summarizes the existing knowledge in classification, prognosis and diagnosis, and summarizes the ECM-driven mechanisms in tumors described so far, aiming to identify new and prognostic biomarkers and novel therapeutic targets in uterine sarcomas.
子宫间质来源肿瘤涵盖一系列罕见肿瘤，从良性的子宫内膜间质结节到侵袭性高级别子宫内膜间质肉瘤及未分化子宫肉瘤。通过分子与免疫组化分析，这类肿瘤的分类已取得进展，但细胞外基质在其生物学中的作用才刚刚开始被认识。细胞外基质不仅提供结构支持，还传递动态信号，调控肿瘤细胞增殖、侵袭、血管生成和免疫逃逸。胶原蛋白、蛋白聚糖、糖胺聚糖及基质细胞蛋白的表达改变重塑了间质结构，并促进疾病进展。此外，基质金属蛋白酶等细胞外基质重塑酶与交联因子共同作用，形成僵硬且促肿瘤发生的微环境，从而促进侵袭和治疗抵抗。这些基质改变还与血管生成、机械转导通路及免疫调节相互交织。迄今研究主要描述了细胞外基质分子在生理性子宫组织功能中的作用，而关于子宫间质来源肿瘤的数据尚显不足。本综述总结了现有关于分类、预后及诊断的知识，并归纳了目前已知的细胞外基质驱动肿瘤机制，旨在为子宫肉瘤寻找新的预后生物标志物及治疗靶点。
肿瘤(癌症)患者之家