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JNCI Journal of the National Cancer Institute 2001 93(15):1171-1173; doi:10.1093/jnci/93.15.1171
© 2001 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 93, No. 15, 1171-1173, August 1, 2001
© 2001 Oxford University Press


BRIEF COMMUNICATION

cis-Activation of the Human Telomerase Gene (hTERT) by the Hepatitis B Virus Genome

Izumi Horikawa, J. Carl Barrett

Affiliation of authors: Laboratory of Biosystems and Cancer, Cancer and Aging Section, Division of Basic Sciences, Center for Cancer Research, National Cancer Institute, Bethesda, MD.

Correspondence to: Izumi Horikawa, Ph.D., National Institutes of Health, Bldg. 40, Rm. 2609, MSC-3020, Bethesda, MD 20892–3020 (e-mail: horikawi@mail.nih.gov).

Telomerase catalyzes the elongation of telomeric repeat DNA to maintain telomere length and structure (1). Although telomerase is a complex composed of a catalytic subunit (hTERT) and an RNA component (hTER), it is the expression of hTERT (2,3) that is the major determinant of telomerase activity in human cells (1,4). Maintaining telomere length by telomerase is associated with human cell immortalization and oncogenesis (1); however, no mutations in the hTERT or hTER telomerase genes have been found in human cancers. Hepatocellular carcinoma is often associated with both telomerase activation and viral infection. Here, we show the cis-activation of the hTERT gene by an insertion of viral DNA into the hTERT promoter region.

A 66-base-pair (bp) sequence within the promoter region of hTERT gene (positions -372 to -307) (Fig. 1Go, . . . [Full Text of this Article]

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