CCND3 LOSS

细胞周期蛋白D在许多癌症类型中被证明是被错误调控的。细胞周期蛋白和它们激活的细胞周期蛋白依赖激酶（CDK）因其致癌特性而建立，在过去十年中一直是主要研究和开发工作的重点。解除细胞周期蛋白调控的方法是广泛变化的，范围从基因组扩增到启动子甲基化变化。据报道，T细胞急性淋巴细胞白血病（T-all）中细胞周期蛋白D3丢失，与其他细胞周期蛋白D的扩增和过度表达相比，这似乎是一个独特的趋势。用靶向治疗性palbociclib治疗细胞周期蛋白D3敲除小鼠显著提高了T-all缺口驱动模型的中位生存率。
Cyclin D has been shown in many cancer types to be misregulated. Well established for their oncogenic properties, the cyclins and the cyclin-dependent kinases (CDK's) they activate have been the focus of major research and development efforts over the past decade. The methods by which the cyclins are deregulated are widely variable, and range from genomic amplification to promoter methylation changes. Cyclin D3 loss has been reported in T-cell acute lymphoblastic leukemia (T-ALL), a seemingly unique trend when compared to the amplifcations and overexpressions of the other cyclin D's. Treating cyclin D3 knockout mice with the targeted therapeutic palbociclib significantly increased the median survival of a Notch-driven model of T-ALL.