PATIENTS WITH CHRONIC LYMPHOCYTIC LEUKEMIA

慢性淋巴细胞白血病患者

• 批准号: 7376477
• 负责人: MARGARET K-H YU
• 金额: $ 2.08万
• 依托单位: UNIVERSITY OF UTAH
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-04-01 至 2007-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7376477
• 关键词: DNA methylation

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.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。DNA甲基化在慢性淋巴细胞白血病中的异常调节这项初步研究的目的是找到Vidaza的剂量，将抑制全球DNA甲基化20%。我们以前的研究表明，地西他滨治疗后，患者的DNA甲基化抑制20%，重新表达法师-1，一种以前被DNA甲基化沉默的肿瘤抗原。一旦我们找到抑制DNA甲基化和重新表达法师-1的Vidaza的最低剂量，我们就可以将联合收割机Vidaza与烷化剂、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。