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Telomere Maintenance and Oncogenesis
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Cancer stem cells and induced pluripotent stem cells (iPSCs) differ from normal tissue stem cells in their ability to maintain telomere length stability and permanent capacity for self-renewal. In normal stem cells these traits gradually decrease with age and/or continuous or accelerated cell division. An origin of cancer cells from committed cells is consistent with a similar mechanism of telomere maintenance in cancer and iPSCs. Telomere shortening/damage is believed to protect cells from malignant transformation but, paradoxically, telomere shortening has been observed repeatedly to precede most cancers and the absence of apoptotic factors like p53 may reveal this inherent favourable role of telomere damage in cancer development. Architectural changes in telomeric chromatin such as those underlying the telomere position effect and others support telomere maintenance of some tumors. Here, we propose that several signaling pathways in conjunction with telomere shortening/damage may result in release of Rap1 from telomeres and its subsequent interaction with the embryonic stem cell marker Zscan4 might support immortalization and malignant transformation of the target cell.
Title: Telomere Maintenance and Oncogenesis
Description:
Cancer stem cells and induced pluripotent stem cells (iPSCs) differ from normal tissue stem cells in their ability to maintain telomere length stability and permanent capacity for self-renewal.
In normal stem cells these traits gradually decrease with age and/or continuous or accelerated cell division.
An origin of cancer cells from committed cells is consistent with a similar mechanism of telomere maintenance in cancer and iPSCs.
Telomere shortening/damage is believed to protect cells from malignant transformation but, paradoxically, telomere shortening has been observed repeatedly to precede most cancers and the absence of apoptotic factors like p53 may reveal this inherent favourable role of telomere damage in cancer development.
Architectural changes in telomeric chromatin such as those underlying the telomere position effect and others support telomere maintenance of some tumors.
Here, we propose that several signaling pathways in conjunction with telomere shortening/damage may result in release of Rap1 from telomeres and its subsequent interaction with the embryonic stem cell marker Zscan4 might support immortalization and malignant transformation of the target cell.
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