University of Heidelberg


09.11.11 10:30 Age: 6 yrs

Forever young according to Plan B


BioQuant researchers unravel molecular components of the alternative lengthening of telomeres (ALT) pathway in tumor cells, published in “Journal of Cell Science”

Normally, the ends of the chromosomes – the telomeres – shorten with every cell division. Once the telomeres become very short the cell stops dividing. Cancer cells manage to circumvent this barrier and divide infinitely, most of them by activating the enzyme telomerase that extends their telomeres again. However, 10 - 15 % of tumors elongate their chromosome ends without telomerase by an alternative telomere lengthening mechanism. It involves DNA repair and recombination processes, and the assembly of PML protein at the telomeres in specific complexes called APBs. Yet, the link between telomere elongation and APBs has remained mysterious. In a recent study, Inn Chung and Karsten Rippe at the BioQuant center succeeded in artificially creating APBs in living cells to study their function. They were able to show that APB formation can induce DNA repair-mediated DNA synthesis at telomeres. Thus, the cancer cells’ “Plan B” to avoid cell death requires APBs, which makes them promising new targets for those tumors that lack telomerase.


Chung, I., Leonhardt, H. & Rippe, K. (2011). De novo assembly of a PML nuclear subcompartment occurs through multiple pathways and induces telomere elongation. J. Cell Sci., doi: 10.1242/jcs.084681.

Press release (English):


Press release (German):


Fluorescence microscopy images of a tumor cell with telomeres stained in green, PML protein in red, and APB complexes indicated by white arrows. The insert shows a high-resolution 4Pi microscopy image of an APB complex with a diameter of ~1 µm (Lang et al. 2010, J. Cell Sci 123, 392-400).

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