Modelling BET inhibitor resistance in acute myeloid leukaemia

急性髓系白血病 BET 抑制剂耐药性建模

• 批准号: nhmrc : 1085015
• 负责人: Prof Mark Dawson
• 金额: $ 51万
• 依托单位: The University of Melbourne
• 依托单位国家: 澳大利亚
• 项目类别: Project Grants
• 财政年份: 2015
• 资助国家: 澳大利亚
• 起止时间: 2015-01-01 至 2018-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/modelling-bet-inhibitor-myeloid-leukaemia/519053
• 关键词: Modelling; BET; inhibitor; resistance; acute

Mutations in epigenetic regulators in AML not only imply a causative role for these proteins in AML but also provide potential targets for therapeutic intervention. One of the most promising epigenetic therapies to have emerged in the last decade are small molecule inhibitors targeted to the Bromodomain and Extra Terminal (BET) family of proteins. This proposal will elucidate the cellular and molecular mechanisms that drive resistance to this new class of drugs

AML中表观遗传调节因子的突变不仅意味着这些蛋白质在AML中的致病作用，而且还提供了治疗干预的潜在靶点。在过去十年中出现的最有前途的表观遗传疗法之一是靶向溴结构域和额外末端（BET）蛋白质家族的小分子抑制剂。这一提议将阐明导致对这类新药产生耐药性的细胞和分子机制