共 108 条
Telomere length maintenance - an ALTernative mechanism
被引:25
作者:
Royle, N. J.
[1
]
Foxon, J.
[1
]
Jeyapalan, J. N.
[1
]
Mendez-Bermudez, A.
[1
]
Novo, C. L.
[1
]
Williams, J.
[1
]
Cotton, V. E.
[1
]
机构:
[1] Univ Leicester, Dept Genet, Leicester LE1 7RH, Leics, England
关键词:
D O I:
10.1159/000167814
中图分类号:
Q2 [细胞生物学];
学科分类号:
071009 ;
090102 ;
摘要:
The Alternative Lengthening of Telomeres (ALT) mechanism is utilised by approximately 10% of human tumours and a higher proportion of some types of sarcomas. ALT+ cell lines and tumours show heterogeneous telomere length, extra-chromosomal circular and linear telomeric DNA, ALT associated promyelocytic bodies (APBs), a high frequency of post-replication exchanges in telomeres (designated as telomere-sister chromatid exchanges, T-SCE) and high instability at a GC-rich minisatellite, MS32 (D1S8). It is clear that there is a link between the minisatellite instability and the mechanism that underpins ALT, however currently the nature of this relationship is uncertain. Single molecule analysis of telomeric DNA from ALT+ cell lines and tumours has revealed complex telomere mutations that have not been seen in cell lines or tumours that express telomerase. These complex telomere mutations cannot be explained by T-SCE but must arise by another inter-molecular process. The break-induced replication (BIR) model that may explain the observed high frequency of T-SCE and the presence of complex telomere mutations is reviewed. Copyright (C) 2008 S. Karger AG, Basel
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页码:281 / 291
页数:11
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