改变的细胞周期停止和基因放大潜力伴随着野生类型p53的丧失
L R Livingstone1, A White, J Sprouse
1Lineberger Comprehensive Cancer Center, Department of Pathology, University of North Carolina, School of Medicine, Chapel Hill 27599-7295.
Cell
|September 18, 1992
概括
野生型p53等位基因的丧失使细胞中高频基因放大成为可能,与正常细胞或具有一个功能性p53等位基因的细胞不同. 这表明p53是p53.
科学领域:
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
- 癌症研究 癌症研究
背景情况:
- 基因放大在转变细胞中很常见,但在正常纤维细胞中却不存在.
- 瘤抑制基因p53在调节基因放大中的作用尚未完全理解.
研究的目的:
- 调查p53等位基因的变化是否足以允许基因放大.
- 确定p53状态对细胞对药物诱导的压力和基因放大反应的影响.
主要方法:
- 基因放大频率在具有不同p53等位基因状态的细胞中进行比较 (野生类型,一种改变,两者都改变).
- 对药物治疗的反应中细胞生长停止的评估.
- 对p53在细胞周期进展中的作用及其与基因放大潜在联系的分析.
主要成果:
- 保留一个野生类型p53等位基因的细胞表现出正常的行为,停止生长,没有放大.
- 缺乏功能性p53等位基因的细胞无法阻止生长,并表现出高频基因放大.
- 具有野生型p53的瘤细胞也显示了基因放大,表明存在替代途径.
结论:
- 野生类型的p53功能的丧失是使高频基因放大成为可能的关键因素.
- 通过细胞周期控制的改变,p53的损失可能会促进放大.
- 其他机制可以绕过p53在基因放大中的调节作用.
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