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ALTered telomeres in response to telomere dysfunction.

机译：响应端粒功能障碍，改变端粒。

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Most cancer cells bypass senescence and acquire immortality by reactivating telomerase, a cellular reverse transcrip-tase that maintain telomeres. Telomerase activity and telomere maintenance confer to cancer cells a unique survival advantage compared with normal somatic cells; these unique traits are very attractive targets in the search for a universal and selective anticancer therapy. Several approaches to inhibit telomerase have been investigated, including telomerase immunotherapy and telomerase inhibition. Strategies to validate targeting telomere integrity have also been examined, including disruption of shelterin, a protein complex that protects telomere structure, expression of a mutated telomerase RNA component that result in the synthesis of defective telomeres or use of G-quadruplex stabilizers.The development of anticancer therapies targeting telomerase and telomeres, however, faces several challenges; one of them is the existence of an unconventional way to maintain telomeres, referred to as the alternative lengthening of telomeres (ALT) pathway
机译：大多数癌细胞通过激活端粒酶（一种维持端粒的细胞逆转录酶）来绕过衰老并获得永生。与正常体细胞相比，端粒酶活性和端粒维持能力赋予癌细胞独特的生存优势;这些独特的特征在寻求通用和选择性的抗癌治疗中非常有吸引力。已经研究了几种抑制端粒酶的方法，包括端粒酶免疫疗法和端粒酶抑制作用。还研究了验证靶向端粒完整性的策略，包括破坏阀蛋白（一种保护端粒结构的蛋白质复合物），表达突变的端粒酶RNA成分（导致有缺陷的端粒合成或使用G-四链体稳定剂）的破坏。然而，针对端粒酶和端粒的抗癌疗法面临着一些挑战。其中之一是存在维护端粒的非常规方法，称为端粒的替代性延长（ALT）途径

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