Affiliation

Department of Pathology and Laboratory Medicine, Center for Viral Oncology, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, USA

Corresponding Author

Christophe Nicot, Professor and Vice Chair, Director Center for Viral Oncology, University of Kansas Medical Center, Department of Pathology, Lied Bldg., Room 2032, 3901 Rainbow Boulevard, Kansas City, KS 66160. Tel: 913-588-6724; Fax: 913-945-6836; E-mail: cnicot@kumc.edu

Citation

Nicot, C., et al. Multiple Pathways Control the Reactivation of Telomerase in HTLV-I-Associated Leukemia. (2015) Int J Cancer Oncol 2(2): 1-8.

Copy rights

© 2015 Nicot, C. This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International License.

Keywords

Abstract

  While telomerase (hTERT) activity is absent from normal somatic cells, reactivation of hTERT expression is a hallmark of cancer cells. Telomerase activity is is required for avoiding replicative senescence and supports immortalization of cellular proliferation. Only a minority of cancer cells rely on a telomerase-independent process known as alternative lengthening of telomeres, ALT, to sustain cancer cell proliferation. Multiple genetic, epigenetic, and viral mechanisms have been found to deregulate telomerase gene expression increasing the risk of cellular transformation. Here, we review the different strategies used by the Human T cell leukemia virus type 1, HTLV-I, to activate hTERT expression and stimulate its enzymatic activity in virally-infected CD4 T cells. The implications of hTERT reactivation in HTLV-I pathogenesis and disease treatment are discussed.