Chang Sandy
Department of Molecular Genetics, MD Anderson Cancer Center, Houston, TX 77030, USA.
Mutat Res. 2005 Aug 25;576(1-2):39-53. doi: 10.1016/j.mrfmmm.2004.08.020.
The telomerase deficient mouse has been invaluable in providing insights into basic questions pertaining to consequences of telomere dysfunction during aging and cancer in the context of the mammalian organism. Studies using this mouse model have demonstrated that cellular responses to telomere dysfunction are fundamentally conserved in both humans and mice, and that the tight regulation of telomere length and telomerase activity in somatic cells may be important in mediating the balance between aging and cancer. Here, I discuss the use of the telomerase null mouse for understanding the contrasting roles of telomeres and telomerase in organismal aging and cancer.
端粒酶缺陷型小鼠对于深入了解哺乳动物机体衰老和癌症过程中端粒功能障碍的相关基本问题具有重要价值。利用这种小鼠模型进行的研究表明，人类和小鼠对端粒功能障碍的细胞反应在根本上是保守的，并且体细胞中端粒长度和端粒酶活性的严格调控对于介导衰老与癌症之间的平衡可能至关重要。在此，我将讨论使用端粒酶缺失小鼠来理解端粒和端粒酶在机体衰老和癌症中的不同作用。
