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Alternative routes to immortality

Every time a cell divides, the ends of chromosomes - the threads of DNA residing in the nucleus - shorten a bit. Once the chromosome ends, called telomeres, become too short, cells normally stop dividing. Scientists led by Karsten Rippe from the German Cancer Research Center (DKFZ) and the BioQuant Center of the Heidelberg University have now discovered how cancer cells make use of specific DNA repair enzymes to extend the telomeres. In this way, they escape the natural stop signal and can divide without limits. The Federal Ministry of Education and Research (BMBF) supports the project as part of the e:Med research initiative.

Osterwald S, Deeg KI, Chung I, Parisotto D, Wörz S, Rohr K, Erfle H & Rippe K (2015). PML induces compaction, partial TRF2 depletion and DNA damage signaling at telomeres and promotes alternative lengthening of telomeres. J Cell Sci, 128 1887-1900 doi: 10.1242/jcs.148296 | Abstract | Reprint (4.3 MB)

Mallm JP & Rippe K (2015). Aurora kinase B regulates telomerase activity via a centromeric RNA in stem cells. Cell Rep 11, 1667-1678. doi: 10.1016/j.celrep.2015.05.015 | Abstract | Reprint (5.9 MB)

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