caa a22 4500 47584582X CHVBK 20180406123913.0 cr unu---uuuuu 170329e20000301xx s 000 0 eng 10.1007/PL00000708 doi (NATIONALLICENCE)springer-10.1007/PL00000708 Cell proliferation, carcinogenesis and diverse mechanisms of telomerase regulation [Elektronische Daten] [G. Krupp*, W. Klapper, R. Parwaresch] Abstract.: Replication of linear genomes is incomplete and leaves terminal gaps. Solutions to this ‘end replication' problem can be traced back to the prebiotic RNA world: ‘fossils' of the presumptive archetypes of telomere structure and of the telomerase enzyme are retained in the terminal structures of some RNA viruses. Telomerase expression in mammals is ubiquitous in embryonic tissues but downregulated in somatic tissues of adults. Exceptions are regenerative tissues and, notably, tumor cells. Telomerase activation is controlled by cellular proliferation, and it is an early step in the development of many tumors. In contrast to mammals, indeterminately growing multicellular organisms, such as fish and crustaceae, maintain telomerase competence in all somatic tissues. In human tumor diagnostics, detection of proliferation markers with monoclonal antibodies is well established, and in this review, the significance of additional telomerase assays is evaluated. Telomerase inhibitors are attractive goals for application in tumor therapy, and telomerase knockout mice have proven that telomere erosion limits the lifespan of cells in vivo. In contrast, telomerase stimulation can be used to expand the potential of cellular proliferation in vitro, with possible applications for transplantation of in vitro expanded human cells, for immortalizing primary human cells as improved tissue models and for the isolation of otherwise intractable products, such as genuine human monoclonal antibodies. Birkhäuser Verlag Basel,, 2000 Key words. Polymerase nationallicence molecular fossils nationallicence rainbow trout nationallicence endometrium nationallicence inhibitors nationallicence Krupp* G. Institute for Hematopathology, Center for Pathology and Applied Cancer Research, Christian-Albrechts-University Kiel, Niemannsweg 11, D-24105 Kiel (Germany), Fax +49 431 597 3426, e-mail: gkrupp@path.uni-kiel.de, DE aut Klapper W. Institute for Hematopathology, Center for Pathology and Applied Cancer Research, Christian-Albrechts-University Kiel, Niemannsweg 11, D-24105 Kiel (Germany), Fax +49 431 597 3426, e-mail: gkrupp@path.uni-kiel.de, DE aut Parwaresch R. Institute for Hematopathology, Center for Pathology and Applied Cancer Research, Christian-Albrechts-University Kiel, Niemannsweg 11, D-24105 Kiel (Germany), Fax +49 431 597 3426, e-mail: gkrupp@path.uni-kiel.de, DE aut https://doi.org/10.1007/PL00000708 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/PL00000708 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Krupp* G. Institute for Hematopathology, Center for Pathology and Applied Cancer Research, Christian-Albrechts-University Kiel, Niemannsweg 11, D-24105 Kiel (Germany), Fax +49 431 597 3426, e-mail: gkrupp@path.uni-kiel.de, DE aut NATIONALLICENCE 700 1- Klapper W. Institute for Hematopathology, Center for Pathology and Applied Cancer Research, Christian-Albrechts-University Kiel, Niemannsweg 11, D-24105 Kiel (Germany), Fax +49 431 597 3426, e-mail: gkrupp@path.uni-kiel.de, DE aut NATIONALLICENCE 700 1- Parwaresch R. Institute for Hematopathology, Center for Pathology and Applied Cancer Research, Christian-Albrechts-University Kiel, Niemannsweg 11, D-24105 Kiel (Germany), Fax +49 431 597 3426, e-mail: gkrupp@path.uni-kiel.de, DE aut Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer