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Malignancy telomerase

Telomerase has been associated with almost 90% of all malignant human cancers, making it the most prominent molecular marker known to date. Because of its association with malignancy, telomerase is also regarded as a novel diagnostic marker and a specific target for gene therapy or chemotherapy. [Pg.126]

Cancer ceDs often have relatively h%h levels of telomerase, preventing the telomeres ftom becoming shortened and contributing to the immortality of malignant cells. [Pg.19]

Kondo Y, Komata T, Kondo S. 2001. Combination therapy of 2-5A antisense agai nst telomerase RNA and cisplatin for malignant gliomas. Int. J. Oncol. 18 1287-92... [Pg.377]

The usefulness of genetic modification of cells which are to be used in engineering tissue is evidenced by non-malignant transformation with human telomerase reverse transcriptase of adrenocortic bovine cells. " ... [Pg.50]

Komata T, Kanzawa T, Kondo Y, Kondo S. Telomerase as a therapeutic target for malignant gliomas. Oncogene 2002 21 656-663. [Pg.516]

Comment. There is an eclat difference between telomere replacement in unicellular eukaryotes (like the ciliates) and somatic cells of multicellular hosts (like the mammals). The ciliates immediately cap with telomeres their chromosome ends after each cell division, whereas the chromosome ends of somatic cells in multicellular hosts remain uncapped, and steadily shorten with each cell division (approx 50 bp per cell divisions). These somatic cells of multicellular hosts undergo senescence and die, at which time stem cells may (or may not) replace them. The tetrahymena cells are rejuvenated and escape senescence due to constant telomere repairs. In that, unicellular eukaryotes (example the ciliates) resemble malignantly transformed somatic cells of the multicellular hosts, except that telomerase action is constitutive (irreversible) in the latter, whereas it can accelerate (at conjugation) and decelerate (after conjugation) in the former. [Pg.124]


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See also in sourсe #XX -- [ Pg.764 ]




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