PML body meets telomere: The beginning of an ALTernate ending?

The unlimited proliferation potential of cancer cells requires the maintenance of their telomeres. This is frequently accomplished by reactivation of telomerase. However, in a significant fraction of tumors an alternative lengthening of telomeres (ALT) mechanism is active. The molecular mechanism of...

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Bibliographic Details
Published in:Nucleus (Austin, Tex.) Tex.), 2012-05, Vol.3 (3), p.263-275
Main Authors: Chung, Inn, Osterwald, Sarah, Deeg, Katharina I., Rippe, Karsten
Format: Article
Language:English
Subjects:
ALT
ALT-associated PML bodies
alternative lengthening of telomeres
Binding
Biology
Bioscience
Calcium
Cancer
Cell
Cell Nucleus Division
cellular immortalization
Cycle
DNA recombination
DNA repair
Humans
Intranuclear Inclusion Bodies - metabolism
Landes
Leukemia, Promyelocytic, Acute - metabolism
Leukemia, Promyelocytic, Acute - pathology
Organogenesis
promyelocytic leukemia nuclear bodies
Proteins
Review
Small Ubiquitin-Related Modifier Proteins - metabolism
Telomere - metabolism
Telomere Homeostasis
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Summary:The unlimited proliferation potential of cancer cells requires the maintenance of their telomeres. This is frequently accomplished by reactivation of telomerase. However, in a significant fraction of tumors an alternative lengthening of telomeres (ALT) mechanism is active. The molecular mechanism of the ALT pathway remains elusive. In particular, the role of characteristic complexes of promyelocytic leukemia nuclear bodies (PML-NBs) with telomeres, the ALT-associated PML-NBs (APBs), is currently under investigation. Here, we review recent findings on the assembly, structure and functions of APBs. It is discussed how genomic aberrations in ALT-positive cancer cells could result in the formation of APBs and in ALT activity. We conclude that they are important functional intermediates in what is considered the canonical ALT pathway and discuss deregulations of cellular pathways that contribute to the emergence of the ALT phenotype.
ISSN:1949-1034
1949-1042
DOI:10.4161/nucl.20326