Research Group Cancer Genome Research

Prof. Dr. Holger Sültmann

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The evolution of cancer goes along with genomic, epigenomic, and transcriptomic mutations. The aims of our research are to identify these alterations, to characterize their roles in tumor progression and therapy resistance, and to translate them into clinical practice. Our activities focus on prostate, kidney, and lung cancer. We apply ultra-high genome and transcriptome sequencing as well as focused screenings to find cancer-related changes on chromatin, genome, and transcriptome (focus on noncoding, i.e. miRNA and lncRNA) levels. We measure the effects of RNA expression on transcriptomes and proteomes in cell lines and mouse models and determine the affected signal transduction pathways. The integration of these data leads to a mechanistic understanding of potentially targetable molecular processes.

FUTURE OUTLOOK
The huge molecular heterogeneity of tumor tissues is a challenge for the therapy decision in individual patients. We use genomics and proteomics technologies to characterize this heterogeneity, to determine cancer specific mutations in blood plasma as a means for tumor monitoring and early detection (liquid biopsy), and to unravel mechanisms of therapy resistance of tumor subclones.

Contact

Prof. Dr. Holger Sültmann
Cancer Genome Research (B063)
Deutsches Krebsforschungszentrum
und Nationales Centrum für Tumorerkrankungen (NCT)
Im Neuenheimer Feld 460
69120 Heidelberg
Tel: +49 (0)6221 565934

Selected Publications

  • Hoefflin R. et al. (2016). Quantitative image analysis and regional whole exome sequencing indicate spatial niche formation but not malignant progression as driving force for intratumoral heterogeneity. Nature Communications, in press
  • Weischenfeldt J. et al. (2013). Integrative genomic analyses reveal androgen-driven somatic alteration landscape in early-onset prostate cancer. Cancer Cell 23, 159-70
  • Gu L. et al. (2015) BAZ2A/TIP5 is involved in epigenetic alterations in prostate cancer and overexpression predicts recurrence. Nature Genetics 47, 22-33
  • Börno S. T. et al. (2012). Genome-wide DNA methylation events in TMPRSS2:ERG Fusion-Negative Prostate Cancers Implicate an EZH2-Dependent Mechanism with miRNA-26a hypermethylation. Cancer Discovery, 2, 1024-35
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