此前已经有老鼠动物研究证实端粒酶的缺失能拮抗癌变。端粒耗损可以促进癌症早期基因组的不稳定，从而刺激引发肿瘤，但同时也可以抑制肿瘤的发生，促进肿瘤细胞生长停滞或死亡。
端粒酶-负责端粒的延长。端粒酶的存在，算是把 DNA 克隆机制的缺陷填补起来，藉由把端粒修复延长，可以让端粒不会因细胞分裂而有所损耗，使得细胞分裂克隆的次数增加。
癌症细胞系的端粒酶水平较低，导致早期病变时的端粒缺失，但随后端粒酶会被激活。因此，缺乏端粒酶的小鼠模型并为揭示端粒酶对细胞癌变的影响。使用一种新的转基因小鼠模型，Begus-Nahrmann研究人员证实了瞬态端粒酶功能障碍是导致肿瘤发生的一个强有力的刺激因子。（生物谷：Bioon.com）
doi:10.1172/JCI63979
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Telomere stability and carcinogenesis: an off-again, on-again relationship
Jennifer J. Wanat and F. Brad Johnson
Previous studies in mice have demonstrated antagonistic effects of telomerase loss on carcinogenesis. Telomere attrition can promote genome instability, thereby stimulating initiation of early-stage cancers, but can also inhibit tumorigenesis by promoting permanent cell growth arrest or death. Human cancers likely develop in cell lineages with low levels of telomerase, leading to telomere losses in early lesions, followed by subsequent activation of telomerase. Mouse models constitutively lacking telomerase have thus not addressed how telomere losses within telomerase-proficient cells have an impact on carcinogenesis. Using a novel transgenic mouse model, Begus-Nahrmann et al. demonstrate in this issue of the JCI that transient telomere dysfunction in telomerase-proficient animals is a potent stimulus of tumor formation.
