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This Article Full Text Full Text (PDF) All Versions of this Article: JME-08-0189v1 43/4/131    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Else, T. PubMed PubMed Citation Articles by Else, T.

Division of Metabolism, Endocrinology and Diabetes, MEND/Department of Internal Medicine, University of Michigan Health System, 1860 BSRB, 109 Zina Pitcher Pl, Ann Arbor, Michigan 48109-2200, USA

(Correspondence should be addressed to T Else; Email: telse{at}umich.edu)

Telomere dysfunction and telomere maintenance mechanisms contribute to major steps of carcinogenesis. Dysfunctional telomeres lead to the generation of genomic aberrations, such as amplifications and deletions. Telomere maintenance mechanisms, such as telomerase activity and alternative telomere lengthening, provide the basis of malignant cell expansion independent of telomere shortening-induced apoptosis or senescence, ensuring tumor survival. Recent advances highlight the importance of these mechanisms in adrenocortical carcinogenesis. In this review, we will summarize the main models of telomere physiology and their impact on adrenocortical tissue maintenance, aging, and carcinogenesis.