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Telomere length maintenance--an ALTernative mechanism.
Cytogenet Genome Res. 2008; 122(3-4):281-91.CG

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.

Authors+Show Affiliations

Department of Genetics, University of Leicester, Leicester, UK. njr@le.ac.ukNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

19188697

Citation

Royle, N J., et al. "Telomere Length Maintenance--an ALTernative Mechanism." Cytogenetic and Genome Research, vol. 122, no. 3-4, 2008, pp. 281-91.
Royle NJ, Foxon J, Jeyapalan JN, et al. Telomere length maintenance--an ALTernative mechanism. Cytogenet Genome Res. 2008;122(3-4):281-91.
Royle, N. J., Foxon, J., Jeyapalan, J. N., Mendez-Bermudez, A., Novo, C. L., Williams, J., & Cotton, V. E. (2008). Telomere length maintenance--an ALTernative mechanism. Cytogenetic and Genome Research, 122(3-4), 281-91. https://doi.org/10.1159/000167814
Royle NJ, et al. Telomere Length Maintenance--an ALTernative Mechanism. Cytogenet Genome Res. 2008;122(3-4):281-91. PubMed PMID: 19188697.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Telomere length maintenance--an ALTernative mechanism. AU - Royle,N J, AU - Foxon,J, AU - Jeyapalan,J N, AU - Mendez-Bermudez,A, AU - Novo,C L, AU - Williams,J, AU - Cotton,V E, Y1 - 2009/01/30/ PY - 2008/09/25/accepted PY - 2009/2/4/entrez PY - 2009/2/4/pubmed PY - 2009/3/12/medline SP - 281 EP - 91 JF - Cytogenetic and genome research JO - Cytogenet. Genome Res. VL - 122 IS - 3-4 N2 - 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. SN - 1424-859X UR - https://www.unboundmedicine.com/medline/citation/19188697/Telomere_length_maintenance__an_ALTernative_mechanism_ L2 - https://www.karger.com?DOI=10.1159/000167814 DB - PRIME DP - Unbound Medicine ER -