Feb 9, 2018

Telomere Length Dynamics and the Evolution of Cancer Genome Architecture

International Journal of Molecular Sciences
Kez ClealDuncan Baird

Abstract

Telomeres are progressively eroded during repeated rounds of cell division due to the end replication problem but also undergo additional more substantial stochastic shortening events. In most cases, shortened telomeres induce a cell-cycle arrest or trigger apoptosis, although for those cells that bypass such signals during tumour progression, a critical length threshold is reached at which telomere dysfunction may ensue. Dysfunction of the telomere nucleoprotein complex can expose free chromosome ends to the DNA double-strand break (DSB) repair machinery, leading to telomere fusion with both telomeric and non-telomeric loci. The consequences of telomere fusions in promoting genome instability have long been appreciated through the breakage-fusion-bridge (BFB) cycle mechanism, although recent studies using high-throughput sequencing technologies have uncovered evidence of involvement in a wider spectrum of genomic rearrangements including chromothripsis. A critical step in cancer progression is the transition of a clone to immortality, through the stabilisation of the telomere repeat array. This can be achieved via the reactivation of telomerase, or the induction of the alternative lengthening of telomeres (ALT) pathway. Whilst...Continue Reading

  • References139
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Mentioned in this Paper

Study
Biochemical Pathway
Telomere Lengthening
Genome
Telomere Shortening
Nucleoproteins
Telomerase Catalytic Subunit
Cell Division
Genomic Stability
Virus Replication

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