了解端粒生物学的复杂动态对于衰老与癌症之间的密切联系非常重要。端粒（染色体末端的保护帽）是这方面的核心角色。虽然它们因复制而逐渐缩短，通过触发 DNA 修复机制来限制肿瘤的扩张，但它也会促进染色体内的致癌变化，从而维持肿瘤的发生。负责维持端粒长度的端粒酶在这方面发挥着核心作用。它在癌细胞中的表达有利于端粒的保存，使它们能够规避短端粒的生长限制作用。有趣的是，端粒酶的影响超出了端粒维持的范围，它通过替代途径参与促进细胞生长就证明了这一点。在这种情况下，炎症会加速端粒缩短，导致端粒功能障碍，而端粒元件也在调节炎症反应中发挥作用。对这种相互作用的认识促进了以端粒酶抑制为中心的新型治疗方法的发展。这篇综述对该领域进行了全面的概述，强调了知识的最新进展以及对理解癌症生物学的影响。

Understanding the complex dynamics of telomere biology is important in the strong link between aging and cancer. Telomeres, the protective caps at the end of chromosomes, are central players in this connection. While their gradual shortening due to replication limits tumors expansion by triggering DNA repair mechanisms, it also promotes oncogenic changes within chromosomes, thus sustaining tumorigenesis. The enzyme telomerase, responsible for maintaining telomere length, emerges as a central player in this context. Its expression in cancer cells facilitates the preservation of telomeres, allowing them to circumvent the growth-limiting effects of short telomeres. Interestingly, the influence of telomerase extends beyond telomere maintenance, as evidenced by its involvement in promoting cell growth through alternative pathways. In this context, inflammation accelerates telomere shortening, resulting in telomere dysfunction, while telomere elements also play a role in modulating the inflammatory response. The recognition of this interplay has promoted the development of novel therapeutic approaches centered around telomerase inhibition. This review provides a comprehensive overview of the field, emphasizing recent progress in knowledge and the implications in understanding of cancer biology.