Autor/Autorin: Valentini Fabio
Dr Valentini graduated at the University of Bologna (Italy) in 1999. One year later he moved to the University of Illinois pursuing a 2-year MS and clinical oncology internship. In 2010 he started his residency in medical oncology for the ECVIM (European College of Veterinary Internal Medicine). Author of several articles in peer-reviewed journals
One of the several differences between a normal and a neoplastic cell is that there is a physiological limit to the number of possible cell replications in the former, whereas it appears to be unlimited in the latter. For this reason, cancer cells are thought to undergo a phenomenon of immortalization. The chromosome extremities contain structurally defined elements called telomeres. In normal somatic cells, each mitotic cycle leads to a reduction of telomere length until a critical point is reached. Telomere erosion to this critical length presents a signal for the cell to arrest further divisions and to undergo cellular senescence or to activate apoptosis. Telomeres that avoid critical shortening could, theoretically, replicate endlessly, thereby immortalizing the cell. One mechanism to restore telomere length is the activation of a specific reverse tranillegalscriptase called telomerase. Up-regulation of the telomerase enzyme provides immortalizing capacity to neoplastic cells.
One of the several differences between a normal and a neoplastic cell is that there is a physiological limit to the number of possible cell replications in the former, whereas it appears to be unlimited in the latter. For this reason, cancer cells are thought to undergo a phenomenon of immortalization. The chromosome extremities contain structurally defined elements called telomeres. In normal somatic cells, each mitotic cycle leads to a reduction of telomere length until a critical point is reached. Telomere erosion to this critical length presents a signal for the cell to arrest further divisions and to undergo cellular senescence or to activate apoptosis. Telomeres that avoid critical shortening could, theoretically, replicate endlessly, thereby immortalizing the cell. One mechanism to restore telomere length is the activation of a specific reverse tranillegalscriptase called telomerase. Up-regulation of the telomerase enzyme provides immortalizing capacity to neoplastic cells.
Dr Valentini graduated at the University of Bologna (Italy) in 1999. One year later he moved to the University of Illinois pursuing a 2-year MS and clinical oncology internship. In 2010 he started his residency in medical oncology for the ECVIM (European College of Veterinary Internal Medicine). Author of several articles in peer-reviewed journals
Über den Autor
Dr Valentini graduated at the University of Bologna (Italy) in 1999. One year later he moved to the University of Illinois pursuing a 2-year MS and clinical oncology internship. In 2010 he started his residency in medical oncology for the ECVIM (European College of Veterinary Internal Medicine). Author of several articles in peer-reviewed journals
Klappentext
One of the several differences between a normal and a neoplastic cell is that there is a physiological limit to the number of possible cell replications in the former, whereas it appears to be unlimited in the latter. For this reason, cancer cells are thought to undergo a phenomenon of immortalization. The chromosome extremities contain structurally defined elements called telomeres. In normal somatic cells, each mitotic cycle leads to a reduction of telomere length until a critical point is reached. Telomere erosion to this critical length presents a signal for the cell to arrest further divisions and to undergo cellular senescence or to activate apoptosis. Telomeres that avoid critical shortening could, theoretically, replicate endlessly, thereby immortalizing the cell. One mechanism to restore telomere length is the activation of a specific reverse tranillegalscriptase called telomerase. Up-regulation of the telomerase enzyme provides immortalizing capacity to neoplastic cells.
