The cell phenotypes of senescence and crisis operate to circumscribe the proliferative potential of mammalian cells, suggesting that both are capable of operating in vivo to suppress the formation of tumors. The key regulators of these phenotypes are the telomeres, which are located at the ends of chromosomes and operate to protect the chromosomes from end-to-end fusions. Telomere erosion below a certain length can trigger crisis. The relationship between senescence and telomere function is more complex, however: Cell-physiological stresses as well as dysfunction of the complex molecular structures at the ends of telomeric DNA can trigger senescence. Cells can escape senescence by inactivating the Rb and p53 tumor suppressor proteins and can surmount crisis by activating a telomere maintenance mechanism. The resulting cell immortalization is an essential component of the tumorigenic phenotype of human cancer cells. Here we discuss how telomeres are monitored and maintained and how loss of a functional telomere influences biological functions as diverse as aging and carcinogenesis.

中文翻译：

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端粒：人类衰老的癌症。

衰老和危机的细胞表型限制了哺乳动物细胞的增殖潜能，这表明两者都能够在体内起作用以抑制肿瘤的形成。这些表型的关键调控因子是端粒，端粒位于染色体的末端，可保护染色体免于端对端融合。端粒侵蚀低于一定长度会引发危机。然而，衰老与端粒功能之间的关系更为复杂：端粒DNA末端的细胞生理应激以及复杂分子结构的功能障碍均可触发衰老。细胞可以通过使Rb和p53肿瘤抑制蛋白失活而逃脱衰老，并可以通过激活端粒维持机制来克服危机。最终的细胞永生化是人类癌细胞致瘤表型的重要组成部分。在这里，我们讨论如何监控和维护端粒，以及功能性端粒的丧失如何影响生物学功能，如衰老和致癌作用。