Telomerase is a ribonucleoprotein that maintains telomere. It is activated in greater than 85% of human neoplasms. Traditionally, reactivation of telomerase during tumorigenesis was thought to be required solely to impart an indefinite lifespan. Recently, however, several studies have suggested that telomerase may contribute to tumorigenesis via an additional mechanism that is independent of its role in telomere lengthening. We sought to identify the region(s) of hTERT that contribute to this non-classical role of telomerase. We proposed to identify such regions by their ability to impart a tumorigenic phenotype in ALT cells transduced with activated Ras. Also, we attempted to develop methods to demonstrate that this role is not dependant of telomerase localizing to the telomere. The strategies employed and the progress gained toward each goal is presented in this thesis.

Thesis (Ph.D.) -- McMaster University, 1997. / Includes bibliographical references (leaves 204-216). Also available via World Wide Web.

Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 4 uppsatser.

Thesis (Ph. D.)--Michigan State University. Dept. of Biochemistry and Molecular Biology, 2006. / Title from PDF t.p. (viewed on Nov. 17, 2008) Includes bibliographical references. Also issued in print.

Thesis (Ph.D.)--Michigan State University. Dept. of Pathobiology and Diagnostic Investigation, 2008. / Title from PDF t.p. (viewed on July 10, 2009) Includes bibliographical references (p. 157-174). Also issued in print.

Thesis (M.S.)--University of Michigan, 2000. / Includes bibliographical references.

Thesis (doctoral)--Lund University, 1997. / Added t.p. with thesis statement inserted.

Thesis (doctoral)--Lund University, 1997. / Added t.p. with thesis statement inserted.

Thesis (M. Phil.)--University of Hong Kong, 2005. / Title proper from title frame. Also available in printed format.

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