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[端粒、端粒酶与癌症的发展]

[Telomeres, telomerase and development of cancer].

作者信息

Andersen T I

机构信息

Avdeling for medisinsk genetikk Ullevål sykehus, Blindern, Oslo.

出版信息

Tidsskr Nor Laegeforen. 1998 May 20;118(13):2043-6.

PMID:9656791
Abstract

The chromosome ends, telomeres, shorten during each cell division due to the inability of DNA polymerase to replicate the ends of linear chromosomes. The telomere length serves as a clock determining the remaining replicative capacity of the cell. After 50-100 doublings, the cell becomes senescent. Rarely, a cell overcomes the senescence blockade, and eventually becomes immortal. Cellular immortalisation is almost always accompanied by the expression of the enzyme telomerase, which synthesises telomeric DNA. Telomerase is present in approximately 85% of malignancies. The detection of telomerase activity in cancer cells represents a possible cancer diagnostic and prognostic tool, and telomerase inhibition may become a novel therapeutic strategy in cancer patients.

摘要

染色体末端,即端粒,在每次细胞分裂过程中都会缩短,这是由于DNA聚合酶无法复制线性染色体的末端所致。端粒长度充当着一个时钟,决定着细胞剩余的复制能力。经过50至100次倍增后,细胞会衰老。极少数情况下,细胞会克服衰老障碍,最终变成永生化细胞。细胞永生化几乎总是伴随着端粒酶的表达,端粒酶可合成端粒DNA。端粒酶大约存在于85%的恶性肿瘤中。检测癌细胞中端粒酶活性是一种可能的癌症诊断和预后工具,抑制端粒酶可能成为癌症患者的一种新型治疗策略。

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