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PML body meets telomere: the beginning of an ALTernate ending?
Nucleus 2012 May-Jun; 3(3):263-75N

Abstract

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.

Authors+Show Affiliations

Research Group Genome Organization & Function, Deutsches Krebsforschungszentrum (DKFZ) and BioQuant, Heidelberg, Germany.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

22572954

Citation

Chung, Inn, et al. "PML Body Meets Telomere: the Beginning of an ALTernate Ending?" Nucleus (Austin, Tex.), vol. 3, no. 3, 2012, pp. 263-75.
Chung I, Osterwald S, Deeg KI, et al. PML body meets telomere: the beginning of an ALTernate ending? Nucleus. 2012;3(3):263-75.
Chung, I., Osterwald, S., Deeg, K. I., & Rippe, K. (2012). PML body meets telomere: the beginning of an ALTernate ending? Nucleus (Austin, Tex.), 3(3), pp. 263-75. doi:10.4161/nucl.20326.
Chung I, et al. PML Body Meets Telomere: the Beginning of an ALTernate Ending. Nucleus. 2012;3(3):263-75. PubMed PMID: 22572954.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - PML body meets telomere: the beginning of an ALTernate ending? AU - Chung,Inn, AU - Osterwald,Sarah, AU - Deeg,Katharina I, AU - Rippe,Karsten, Y1 - 2012/05/01/ PY - 2012/5/11/entrez PY - 2012/5/11/pubmed PY - 2012/12/10/medline SP - 263 EP - 75 JF - Nucleus (Austin, Tex.) JO - Nucleus VL - 3 IS - 3 N2 - 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. SN - 1949-1042 UR - https://www.unboundmedicine.com/medline/citation/22572954/PML_body_meets_telomere:_the_beginning_of_an_ALTernate_ending L2 - http://www.tandfonline.com/doi/full/10.4161/nucl.20326 DB - PRIME DP - Unbound Medicine ER -