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Oncology

Term: 01.03.2020 – 31.08.2022

Axin is a key negative regulator of the oncogenic Wnt/beta-catenin pathway scaffolding the beta-catenin destruction complex. We suggest that the newly found anchoring of axin to microtubules (MTs) is of functional importance for regulating the pathway. We will (i) describe the dynamics of axin association with MTs; (ii) determine the biochemical basis of this interaction and its regulation by phosphorylation; and (iii) define the functional role of axin anchoring to MTs in Wnt signaling.

Principal Investigator
Prof. Dr. Jürgen Behrens
Phone: +49 9131 85-29109
E-Mail: juergen.behrens@fau.de
Principal Investigator
Dr. Dominic Bernkopf
Phone: +49 9131 85-29122
E-Mail: dominic.bernkopf@fau.de

Term: 16.03.2020 – 15.09.2022

Oncogene-induced senescence (OIS) was recently introduced as a strong tumor suppressive mechanism seen e.g. in development of nevi out of melanocytes after BRAF mutation. Tumor cells like melanoma obviously can overcome these limiting mechanisms by further changes, however the molecular mechanisms leading to and overcoming OIS are just being started to be understood. We aim to understand the role of cell adhesion processes and mechanotransduction in induction and overcoming OIS.

Principal Investigator
Prof. Dr. Anja Bosserhoff
Phone: +499131 85-24190
E-Mail: anja.bosserhoff@fau.de

Term: 01.03.2020 – 31.08.2020

Neuropeptide Y (NPY) and its receptors represent a highly conserved system which is involved in cancer-related hallmarks. However, the impact of the NPY-system on hepatocellular carcinoma (HCC) remains unclear. The aims of this study are i) to unravel the role of NPY-receptor/NPY-crosstalk in resistance to tyrosine kinase inhibitors such as sorafenib and lenvatinib in HCC, and ii) to analyze the unknown role of the NPY-system as a potential major determinant of immune-escape in HCC.

Principal Investigator
Dr. Dr. Peter Dietrich
Phone: +49 9131 85-45221
E-Mail: peter.dietrich@uk-erlangen.de

Despite the improvement through tyrosine kinase inhibitors (TKIs), treatment resistance, relapse and therapy-induced side effects are central problems of CML therapy. Our interdisciplinary project addresses the question whether and how TKIs alter CML cell metabolism and induce synthetic lethality in combination with compounds specifically targeting metabolic pathways. Our approach could help to improve efficacy and reduce side effects of CML treatment in pediatric and adult patients alike.

Principal Investigator
Prof. Dr. Markus Metzler
Phone: +49 9131 85-33117
E-Mail: markus.metzler@uk-erlangen.de
Principal Invertigator
Prof. Dr. Dimitrios Mougiakakos
E-Mail: dimitrios.mougiakakos@uk-erlangen.de

Term: 01.05.2020 – 31.10.2022

We have identified PU.1 as a key regulator of fibroblast polarization. Its role in colorectal carcinoma (CRC) is unknown. We will address the following aims: (1) characterization of cancer-associated fibroblast (CAF) heterogeneity in CRC, (2) analysis of CAF polarization-dependent fibrocrine effects in vitro and (3) in experimental animal models, and (4) validation of the results in CRC tissues. Deciphering the role of fibroblast polarization in CRC may provide a new target for therapy.

Principal Investigator
Dr. Andreas Ramming
Phone: +49 9131 85-34742
E-Mail: andreas.ramming@uk-erlangen.de
Principal Investigator
Prof. Dr. Michael Stürzl
Phone: +49 9131 85-39520
E-Mail: michael.stuerzl@uk-erlangen.de

The renal cancer risk SNP on chromosome 14q24.2 creates a novel Hypoxia inducible transcription factor (HIF)-binding DNA element in an intronic region of the DPF3 gene, a member of the SWI/SNF chromatin remodelling complex. DPF3 is upregulated in a SNP- and HIF-dependent fashion in renal tubular cells. We investigate the regulation of DPF3 in renal cells and cancer as well as its contribution to global chromatin status and transcription factor binding to critical DNA regions.

Principal Investigator
PD Dr. Johannes Schödel
Phone: +49 9131 85-39560
E-Mail: johannes.schoedel@uk-erlangen.de

Term: 01.03.2020 – 31.08.2020

This proposal will focus on the molecular basis of tumor inflammation of two different advanced cancers; Bladder cancer (MIBC) and Ovarian cancer (OVCA) with poor survival outcomes and high recurrence rates. Endogenous retrovirus (ERV) activations are linked with innate immunity and tumor inflammation. We will correlate patient immune signatures with ERVs and determine the functional role of ERVs, including dsRNA and RNA/DNA intermediates using tumors, cell lines and tumoroids of MIBC and OVCA.

Principal Investigator
Prof. Dr. Reiner Strick
Phone: +49 9131 85-36671
E-Mail: reiner.strick@uk-erlangen.de
Principal Investigator
Prof. Dr. Arndt Hartmann
Phone: +49 9131 85-22286
E-Mail: arndt.hartmann@uk-erlangen.de