Background/Objectives: As cells divide, telomeres shorten through a phenomenon known as telomere attrition, which leads to unavoidable senescence of cells. Unprotected DNA exponentially increases the odds of mutations, which can evolve into premature aging disorders and tumorigenesis. There has been growing academic and clinical interest in exploring this duality and developing optimal therapeutic strategies to combat telomere attrition in aging and cellular immortality in cancer. The purpose of this review is to provide an updated overview of telomere biology and therapeutic tactics to address aging and cancer. Methods: We used the Rayyan platform to review the PubMed database and examined the ClinicalTrial.gov registry to gain insight into clinical trials and their results. Results: Cancer cells activate telomerase or utilize alternative lengthening of telomeres to escape telomere shortening, leading to near immortality. Contrarily, normal cells experience telomeric erosion, contributing to premature aging disorders, such as Werner syndrome and Hutchinson–Gilford Progeria, and (2) aging-related diseases, such as neurodegenerative and cardiovascular diseases. Conclusions: The literature presents several promising therapeutic approaches to potentially balance telomere maintenance in aging and shortening in cancer. This review highlights gaps in knowledge and points to the potential of these optimal interventions in preclinical and clinical studies to inform future research in cancer and aging.
背景/目的：随着细胞分裂，端粒会通过一种称为端粒磨损的现象逐渐缩短，最终导致细胞不可避免地衰老。未受保护的DNA会显著增加突变几率，进而可能演变为早衰性疾病和肿瘤发生。学术界和临床领域对于探索这一双重性并制定最佳治疗策略以应对衰老中的端粒磨损和癌症中的细胞永生现象日益关注。本综述旨在提供关于端粒生物学及其在应对衰老和癌症方面治疗策略的最新概述。方法：我们利用Rayyan平台检索PubMed数据库，并查阅ClinicalTrial.gov注册库以深入了解临床试验及其结果。结果：癌细胞通过激活端粒酶或利用端粒替代延长机制来逃避端粒缩短，从而实现近乎永生。相反，正常细胞经历端粒侵蚀，导致（1）早衰性疾病，如沃纳综合征和哈钦森-吉尔福德早衰综合征，以及（2）衰老相关疾病，如神经退行性疾病和心血管疾病。结论：现有文献提出了几种有前景的治疗方法，可能平衡衰老过程中的端粒维持与癌症中的端粒缩短。本综述指出了当前知识的空白，并强调了这些优化干预措施在临床前和临床研究中的潜力，为未来癌症和衰老研究提供方向。
肿瘤(癌症)患者之家