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Research topics

1. Identification and characterization of novel lncRNAs and RBPs in cancer
RBPs and lncRNAs can modulate gene expression on multiple levels (epigenetic, splicing, post-transcriptional) and therefore have the potential to influence tumor – stroma crosstalk, e.g. by controlling the expression of cell surface receptors and signaling molecules (cytokines, chemokines). Own studies have shown that the long non-coding RNA HULC is highly upregulated in human hepatocellular carcinoma and is regulated by the oncofetal RBP IGF2BP1 (Haemmerle et al., 2014). Additionally, we characterized the function of MALAT-1 in lung cancer in vitro and in vivo and identified this lncRNA as an important RNA responsible for lung cancer metastasis (Gutschner et al., 2013).

In our lab, we aim to identify lncRNAs-RBPs networks found in specific subtypes of pancreatic, ovarian and colorectal cancer in order to identify tumor specific but also common deregulated lncRNAs and RBPs, which are implicated in pathways crucial for immunological regulation and epithelial to mesenchymal transition. Here, we are specifically interested in how deregulation of these RNAs and proteins shape the composition of the tumor immune microenvironment and subsequently regulate tumor growth and metastasis in vivo.

 

2. Role of platelets, thrombocytosis and coagulation factors in tumor growth and metastasis
Approximately 40% of cancer patients have an increased platelet blood count, i.e. thrombocytosis, at time of their diagnosis. Interestingly, especially pancreatic cancer patients have a high risk of developing thrombocytosis and as a consequence potentially severe thromboembolic complications. Vice versa, there is a six-fold higher relative risk for the subsequent diagnosis of an occult pancreatic carcinoma after the occurrence of a thromboembolic event. This suggests that platelets and thromboembolic complications might be used as cancer biomarkers as well as clinical targets. Although an association of thromboembolism and pancreatic cancer was first made in the 1930s, the relative contribution of platelets and the coagulation system on tumor growth and metastasis in vivo has not been clarified in detail.

We would like to gain a mechanistic understanding of the role of platelets, thrombocytosis and the coagulation system in pancreatic cancer. Therefore, state-of-the-art techniques like RNA sequencing, multispectral imaging and CRISPR/Cas9 genome editing will be used in conjunction with translational studies in mouse models of pancreatic cancer to unravel the biological significance and molecular function of platelets and the coagulation system in tumor growth and metastasis. Furthermore, translational and pre-clinical studies using human tissue samples and animal models will investigate the role of platelets in the regulation of the local immune microenvironment and will evaluate the clinical efficacy of combined anti-platelet and immune checkpoint inhibitor therapies in vivo. This will deepen our understanding of the interplay between pancreatic cancer cells and platelets, and might identify novel, tumor microenvironment-directed therapeutic opportunities for this devastating cancer disease.