Telomeres are the protective end caps of eukaryotic chromosomes and they determine the proliferative lifespan of somatic cells, as the protectors of cell replication. Telomere length in leucocytes reflects telomere length in other somatic cells. Leucocyte telomere length can be a biomarker of human ageing. The risk of diseases associated with reduced cell proliferation and tissue degeneration, including aging or aging-associated diseases, such as dyskeratosis congenita, cardiovascular diseases, pulmonary fibrosis and aplastic anemia, is correlated with an increase in the shortening of telomeres. On the other hand, the risk of diseases that are associated with increased proliferative growth, including major cancers, is correlated with long telomeres. In most of the cancers, a telomere maintenance mechanism during DNA replication is essential. The reactivation of the functional ribonucleoprotein holoenzyme complex (telomerase) starts the cascade from normal and premalignant somatic cells to advanced malignant cells. Telomerase is overexpressed during the development of cancer and embryonic stem cells, through controlling genome integrity, cancer formation and stemness. Cancer cells have mechanisms to maintain telomeres to avoid initiation of cellular senescence or apoptosis, and halting cell division by critically short telomeres. Modulation of the human telomerase reverse transcriptase is the rate-limiting step for the production of functional telomerase and telomere maintenance. The human telomerase reverse transcriptase promoter promotes its gene expression only in tumor cells, but not in normal cells. Some cancers activate an alternative expansion of telomeres maintenance mechanism via DNA recombination to reduce the shortening of their telomeres. Not only heritability but also oxidative stress, inflammation, environmental factors, and therapeutic interventions have an effect on telomere shortening, explaining the variability in telomere length across individuals. There have been a large number of publications, which correlate human diseases with progressive telomere shortening. Telomere length of an individual at birth is also important to follow up telomere shortening, and it can be used as a biomarker for healthy aging. On the other hand, understanding of cellular stress factors, which affect stem cell behavior, will be useful in regeneration or treatment of cancer and age-associated diseases. In this review, we will understand the connection between stem cell and telomere biology, cancer, and aging-associated diseases. This connection may be useful for discovering novel drug targets and improve outcomes for patients having cancer and aging-associated diseases.

端粒是真核染色体的保护端帽，它们决定体细胞的增殖寿命，作为细胞复制的保护者。白细胞中的端粒长度反映了其他体细胞中的端粒长度。白细胞端粒长度可以作为人类衰老的生物标志物。与细胞增殖减少和组织退化相关的疾病风险，包括衰老或衰老相关疾病，如先天性角化不良、心血管疾病、肺纤维化和再生障碍性贫血，与端粒缩短的增加相关。另一方面，与增殖性生长增加相关的疾病风险，包括主要癌症，与长端粒有关。在大多数癌症中，DNA 复制过程中的端粒维持机制是必不可少的。功能性核糖核蛋白全酶复合物（端粒酶）的重新激活启动了从正常和恶变前体细胞到晚期恶性细胞的级联反应。通过控制基因组完整性、癌症形成和干细胞，端粒酶在癌症和胚胎干细胞的发育过程中过度表达。癌细胞具有维持端粒的机制，以避免启动细胞衰老或凋亡，并通过极短的端粒阻止细胞分裂。人类端粒酶逆转录酶的调节是产生功能性端粒酶和端粒维持的限速步骤。人端粒酶逆转录酶启动子仅在肿瘤细胞中促进其基因表达，而在正常细胞中不促进其基因表达。一些癌症通过 DNA 重组激活端粒维持机制的另一种扩展，以减少其端粒的缩短。不仅遗传力而且氧化应激、炎症、环境因素和治疗干预都会影响端粒缩短，从而解释了个体端粒长度的可变性。已经有大量出版物将人类疾病与进行性端粒缩短相关联。出生时个体的端粒长度对于跟踪端粒缩短也很重要，它可以用作健康老龄化的生物标志物。另一方面，了解影响干细胞行为的细胞应激因素将有助于癌症和年龄相关疾病的再生或治疗。在这次审查中，我们将了解干细胞和端粒生物学、癌症和衰老相关疾病之间的联系。这种联系可能有助于发现新的药物靶点并改善患有癌症和衰老相关疾病的患者的预后。