治疗相关性骨髓增生异常（t-MN）是用于治疗恶性和非恶性疾病的细胞毒性治疗（CT）的迟发并发症。历史上，t-MN被认为是CT诱导的DNA损伤直接导致正常造血干细胞（HSPC）的结果。然而，我们现在知道在t-MN发展中，治疗引起的HSC突变并不是唯一的因素，其他因素可能有助于t-MN的发生。在这一领域，已知的驱动因子之一是骨髓微环境（BMM），尤其是骨髓间充质干细胞（BM-MSC），其在t-MN发病机制中的作用是本次综述的主题。BM-MSC在生理上通过造血-基质相互作用和细胞因子的产生来支持HSC的维持、自我更新和分化。此外，BM-MSC还维持BM免疫微环境的稳定性，并通过减少HSC受到的应激刺激而减轻损伤。在t-MN背景下，化疗/放疗可能会对BM-MSC造成损伤，并通过促进促炎反应、克隆选择和/或产生可能有利于恶性造血的因子来改变BM-MSC的功能。在过去的十年中，已经发现与新发和治疗相关MN患者分离的BM-MSC与正常BM-MSC相比，具有较低的增殖和克隆能力、形态改变、增加的衰老、缺陷的成骨分化潜能、受损的免疫调节特性以及支持HSC生长和分化的能力下降。虽然对体外扩增的t-MN-MSC的遗传和基因表达谱的理解仍然有限且存在争议，但在预后和治疗方面，它作为一个吸引许多研究人员的动力源具有潜在的作用。

Therapy-related myeloid neoplasms (t-MN) are a late complication of cytotoxic therapy (CT) used in the treatment of both malignant and non-malignant diseases. Historically, t-MN has been considered to be a direct consequence of DNA damage induced in normal hematopoietic stem or progenitor cells (HSPC) by CT. However, we now know that treatment-induced mutations in HSC are not the only players involved in t-MN development, but additional factors may contribute to the onset of t-MN. One of the known drivers involved in this field is the bone marrow microenvironment (BMM) and, in particular, bone marrow mesenchymal stem cells (BM-MSC), whose role in t-MN pathogenesis is the topic of this mini-review. BM-MSCs, physiologically, support HSC maintenance, self-renewal, and differentiation through hematopoietic-stromal interactions and the production of cytokines. In addition, BM-MSCs maintain the stability of the BM immune microenvironment and reduce the damage caused to HSC by stress stimuli. In the t-MN context, chemo/radiotherapy may induce damage to the BM-MSC and likewise alter BM-MSC functions by promoting pro-inflammatory response, clonal selection and/or the production of factors that may favor malignant hematopoiesis. Over the last decade, it has been shown that BM-MSC isolated from patients with de novo and therapy-related MN exhibit decreased proliferative and clonogenic capacity, altered morphology, increased senescence, defective osteogenic differentiation potential, impaired immune-regulatory properties, and reduced ability to support HSC growth and differentiation, as compared to normal BM-MSC. Although the understanding of the genetic and gene expression profile associated with ex vivo-expanded t-MN-MSCs remains limited and debatable, its potential role in prognostic and therapeutic terms is acting as a flywheel of attraction for many researchers.