MDS为恶性血液系统疾病，课题组前期研究发现，经典Wnt通路异常激活参与MDS发生发展，该通路拮抗基因SOX7甲基化状态与MDS患者预后密切相关，同时发现甲基化修饰介导SOX7表达沉默。因部分MDS患者出现异常共表达CD34/CD117骨髓细胞，且该群细胞具有较高的转白风险和预示较差预后，我们将以此为标记分选RAEB-1和RAEB-2患者骨髓异常细胞，利用慢病毒转染增加其SOX7基因表达，以从体外功能学研究评价SOX7表达沉默对患者骨髓原始细胞的增殖、细胞周期及细胞凋亡的影响，并推测SOX7可影响患者原始细胞的分化。试验最终将证明SOX7在患者骨髓原始细胞中通过抑制β-catenin与TCF/LEF结合来调控经典Wnt信号通路下游基因（cyclinD1、c-myc及survivin）表达，而参与疾病的发生发展。阐明SOX7发挥预后价值的可能机制，为寻找MDS新的预后标记及治疗靶点提供依据。

Myelodysplastic syndrome (MDS) is a group of hematopoietic malignancies. Our previous study revealed that the canonical Wnt/β-catenin pathway was activated in the occurrence and development of MDS. Also, the methylation of a negative regulator of the Wnt signaling pathway, SOX7, represses its expression, and is correlated with the prognosis of MDS. Co-expression of CD34/CD117 had been found in part of MDS patients, stands for poor prognosis and associates with a higher risk of leukemic transformation.We will increase the expression of SOX7 in CD34+/CD117+ marrow cells extracted by flow cytometry through transduction with a lentivirus vector. We will test, in vitro, the effect of SOX7 on cell apoptosis, proliferation, colony formation and differentiation in CD34+/CD117+ marrow cells of RAEB-1 and RAEB-2. SOX7 is involved the development of MDS by inhibiting the combination of β-catenin and TCF/LEF, thus regulating the expression of downstream genes（cyclinD1、c-myc and survivin）of the Wnt signaling pathway. Therefore, elucidating the prognostic value of SOX7 may provide novel evidence for prognostic marker and therapeutic.