PATIENTS WITH CHRONIC LYMPHOCYTIC LEUKEMIA

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。DNA甲基化在慢性淋巴细胞白血病中异常调节。这项初步研究的目的是找到能将DNA甲基化抑制20%的剂量。我们之前的研究表明，在接受地西他滨治疗后，患者的整体DNA甲基化抑制了20%，重新表达MAGE-1，这是一种以前被DNA甲基化沉默的肿瘤抗原。一旦我们找到抑制DNA甲基化和重新表达MAGE-1的最低剂量的维达扎，我们就可以将维达扎与烷基化剂、蛋白酶体抑制剂、单克隆抗体等药物联合使用，使慢性淋巴细胞白血病对化疗更敏感。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. DNA methylation is aberrantly regulated in chronic lymphocytic leukemia. This pilot study aims to find the dose of Vidaza that will inhibit global DNA methylation by 20%. We previously showed that inhibition of global DNA methylation by 20% in patients after treatment with decitabine re-expressed MAGE-1, a tumor antigen previously silenced by DNA methylation. Once we find the lowest dose of Vidaza which inhibits DNA methylation and re-expresses MAGE-1, we may be able to combine Vidaza with drugs like alkylators, proteasome inhibitors, monoclonal antibodies and make chronic lymphocytic leukemia more sensitive to chemotherapy.