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Title: Telomere length maintenance--an ALTernative mechanism.
Authors: Royle, NJ
Foxon, J
Jeyapalan, JN
Mendez-Bermudez, A
Novo, CL
Williams, J
Cotton, VE
First Published: 2008
Citation: CYTOGENET GENOME RES, 2008, 122 (3-4), pp. 281-291
Abstract: 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.
DOI Link: 10.1159/000167814
eISSN: 1424-859X
Type: Journal Article
Appears in Collections:Published Articles, Dept. of Genetics

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