Katharina Deeg

Research Interest

Cancer cells require a telomere maintenance mechanism (TMM) to avoid cellular senescence and apoptosis induced by replicative shortening of their chromosome ends. In 25-60% of sarcomas as well as 5-15% of carcinomas telomere repeats are extended by an alternative lengthening of telomeres (ALT) mechanism that operates via DNA repair and recombination processes. However, the precise mechanism is still poorly understood. The presence of ALT can serve as a prognostic marker in some cancer types and thus be valuable for patient stratification. Since ALT is a mechanism that is unique to cancer cells, it also represents an ideal target for novel anti-cancer drugs.

ALT positive tumors and cell lines are characterized by heterogeneous telomere lengths, telomere recombination, high levels of extrachromosomal telomere repeats (ECTRs) and colocalizations of PML and telomeres, termed ALT-associated PML bodies (APBs). We have recently shown that APBs have an essential function in telomere clustering and elongation.

In addition, recent reports have reported high levels of the telomeric repeat-containing RNA (TERRA) in ALT positive cell lines when compared to telomerase positive cell lines. TERRA is transcribed in a subtelomere to telomere direction and ranges in length from 100 bp to 9 kb. It has been proposed to be involved in telomere homeostasis and heterochromatin formation, but its precise function remains elusive.

Interestingly, mutations in the chromatin remodeler ATRX have been shown to have a high correlation with ALT, but loss of ATRX is not sufficient to activate the ALT mechanism.

My project aims at elucidating the functional relevance of TERRA, APBs and ATRX for the ALT mechanism. Moreover, telomere maintenance mechanisms are investigated in pediatric glioblastoma (GBMs), a tumor entity which has an unsual high prevalence of ALT and furthermore harbors recurrent mutations in the histone variant H3.3. A special focus also lies on the identifcation of TMMs in primary tumor samples.

The approach outlined above will advance our understanding of the ALT mechanism and advance ALT identification in a clinical setting. This will potentially provide new therapeutic approaches to target cancer cells, in which the ALT mechanism is active.

Scientific Background

  • Since 01/2016: PostDoc in the Research Group Genome Function and Organization (PD Dr. Karsten Rippe), DKFZ
  • 01/2012 - 12/2015: PhD student in the Research Group Genome Function and Organization (PD Dr. Karsten Rippe), DKFZ
  • PhD Thesis Titel: Identifying drivers and suppressors of the alternative lengthening of telomeres (ALT) pathway
  • 09/2009 - 10/2011: Master of Science, Study Program Molecular Biotechnology at the University of Heidelberg
  • Master Thesis in the group of Prof. Dr. Magnus von Knebel Doeberitz, Department of Applied Tumorbiology, University Hospital Heidelberg

    Title: “Methylation pattern of the HPV16 upstream regulatory region in cervical lesions at different stages of progression”

  • 01/2010 - 06/2010: Visiting student at the Karolinska Institutet, Stockholm, Sweden


Osterwald, S., Deeg, K.I., Parisotto, D., Wörz, S., Rohr, K., Erfle, H. and Rippe, K. (2015). PML induces compaction, TRF2 depletion and DNA damage signaling at telomeres and promotes their alternative lengthening. J. Cell. Sci. 128, 1887–1900.

Chung, I., Osterwald, S., Deeg, K.I., and Rippe, K. (2012) PML body meets telomere: the beginning of an ALTernate ending? (Review) Nucleus, Vol.3, Issue 3.

Eichhorn, T., Dolimbek, B. Z., Deeg, K., Efferth, T., & Atassi, M. Z. (2012). Inhibition in vivo of the activity of botulinum neurotoxin A by small molecules selected by virtual screening. Toxicon, 60(6), 1180–1190.