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University Hospital of Urology

Univ.-Prof. Wolfgang Horninger
Univ.-Prof. Wolfgang Horninger
University Hospital of Urology

Anichstrasse 35
A-6020 Innsbruck

Phone: +43 512 504 24811
Fax: +43 512 504 8365

Research Branch (ÖSTAT Classification)

302055, 302086, 302091


bladder, cancer, cancer drugs, Immunology, kidney, and Prostate

Research Focus

Our research is focused on basic and clinical aspects of common urological cancers, in particular prostate, bladder, and renal. On the one hand, we are interested in biomarkers that improve diagnosis and monitoring success of therapies for malignant diseases. Furthermore, we attempt to better understand therapy resistance and to identify novel drug targets in urological malignancy.

General Facts

Research groups are engaged in studies on optimizing screening for detection of localized prostate cancer which could be cured and on the possibilities to reduce overtreatment. In advanced prostate cancer, the androgen receptor is a target for therapies which prevent tumor growth in vitro and in vivo. Androgen receptor-associated proteins such as p300 contribute to the progression towards castration therapy resistance. Androgen receptor variants which are activated in the absence of ligand are frequently expressed in therapy-resistant disease. Similarly, glucocorticoid receptors also play a role in therapy resistance in prostate cancer. Improvement of diagnosis and therapy monitoring in prostate cancer could be achieved by analyses of circulating tumor cells in body fluids and tissue. Our research also includes analysis of tumor microenvironment and its influence on cancer cells. In urothelium cancer, we investigate potential targets associated with the muscle-invasive phenotype and their role in chemotherapy resistance. We also investigate specific receptors of human macrophages which influence anti-inflammatory and pro-angiogenic responses. We use a variety of modern techniques and co-operate with other groups from the Medical University in Innsbruck and several foreign universities.


Exploiting the Tumor microenvironment in prostate cancer (I. Heidegger)

We recently performed comprehensive scRNA-seq based profiling of the PCa tumor-microenvironment (TME) of four PCa patients demonstrating that 1) the applied technique is feasible in PCa; 2) all TME subpopulations are represented; 3) genes are differentially expressed in cancerous vs. normal subpopulations (e.g. tumor endothelial cells vs normal endothelial cells). In addition, our analysis identified novel PCa tumor endothelial targets and highlights CXCR4/CXCL12 interaction as a potential novel target to interfere with tumor angiogenesis in PCa. Currently, we investigate age-related changes in the prostate microenvironment as we postulate that late-onset PCa represents a diverging clinical phenotype, as the TME is heterogeneous comprising different subpopulations with distinct transcriptomic fingerprints depending on patients age. In addition our academic research program aims to identify predictive TME-based biomarkers in metastatic hormone sensitive PCa patients treated by hormonal therapy allowing a novel area of understanding of dynamic TME modulation by therapy pressure.

Collagen pathway in prostate cancer (I. Heidegger)

Current PCa research focusses on tumor microenvironment alterations including non-cellular components termed “extracellular matrix”. We recently found that the collagen biosynthesis pathway is significantly altered in PCa and might represent an attractive diagnostic and even therapeutic target. Collagen-high patients defined by proteo-transcriptomic analyses revealed a significant association to inferior survival rates. Of note, we were able to identify a non-invasive biomarker for altered collagen metabolism in PCa by quantification of urinary collagen fragments.

Biomarkers for therapy response in metastatic PCa (I. Heidegger, M. Kafka)

Treatment landscape of metastatic PCa significantly changed in the past years. Thus we recently compared clinical outcomes of Docetaxel versus new hormonal therapy (NHT) in the real-world setting and elaborated biomarkers predicting clinical outcome. Summarizing, we observed a trend towards a higher benefit of NHT as first-line treatment compared to Docetaxel in men with mHSPC. Of note, a PSA-Nadir ≤ 0.05 ng/ml or a TSH-increase during therapy were predictors for therapy response.
Currently, we explore biomarkers for therapy response to PSMA Lutetium therapy, a highly innovative treatment approach for metastatic castration resistant PCa (mCRPC).
Moreover, we found that KDM5D is a promising novel biomarker predicting response to docetaxel chemotherapy as early as at the localization of the disease, thus potentially avoiding metastatic biopsies in the mCRPC stage of disease.

Biomarkers for PCa detection (I. Heidegger, M. Kafka)

Prostate-specific antigen (PSA)-based detection of PCa often leads to negative biopsy results or detection of clinically insignificant PCa. Thus, we evaluated the accuracy of Proclarix, a novel blood-based diagnostic test to help in biopsy decision-making in this challenging patient population and highlighted its potential to accurately rule out clinically significant prostate cancer, and therefore to reduce the number of unneeded biopsies a multicenter setting.
Currently, we are testing the impact of Prolaris, a genomic test that analyzes changes in 46 genes in prostate biopsy tissue, for detection upgrading in patients treated by active surveillance.

Androgen receptor coactivators and novel targets in prostate cancer (Z. Culig, F. Handle, T. Furlan, C. Andolfi)

Previously, we demonstrated that the histone acetyltransferases p300 and CBP are up-regulated during androgen ablation in prostate cancer. They are also highly expressed in specimens from patients who received therapy. We show that inhibitors of these coactivators down-regulated androgen receptor activity in prostate cancer cell lines and their derivatives generated during androgen ablation therapy. These coactivators are implicated in regulation of genes related to ribosome and MYC activity. Thus, inhibition of p300 and CBP may contribute to therapy, which interferes with resistance to the non-steroidal anti-androgen enzalutamide. We also identified atypical kinase RIOK1 as a possible target in advanced prostate cancer. Its inhibition causes reduction of proliferation and induction of apoptosis in cellular models. Our group also investigates the role of a component of the MED complex, MED12 which regulates proliferation of androgen receptor-positive and androgen receptor-negative cancer cells.

Biomarkers and preventive agents in prostate cancer (I. Eder-Neuwirt, M. Kafka, M.Ladurner)

In one of our recent projects, we have concentrated on the establishment of a metabolic profile for the early detection of prostate cancer with the aim to reduce the number of unnecessary prostate biopsy using NMR technology. So far, data are promising in distinguishing patients with an elevated PSA but a negative biopsy from those with a positive biopsy. In addition, we are interested in finding novel treatment options for metastatic prostate cancer (mPCa). In this regard, in addition to established cell culture models, we also use patient-derived circulating tumors cells (CTCs) and plasma to investigate molecular changes of tumor cells during therapy in advanced stages of the disease. We have recently shown that cholesterol metabolism plays an essential role in mPCa, and that cholesterol-lowering drugs (statins) and/or inhibitors against AKR1C3, a key molecule in steroid biosynthesis, could be potentially useful drugs in the future.

The impact of glucocorticoid administration on prostate cancer progression and therapy resistance (M. Puhr, F. Handle, I. Heidegger)

The glucocorticoid receptor (GR) is a prime suspect for acquired therapy resistance, as prostate cancer (PCa) cells are able to increase GR signaling during anti-androgen therapy and thereby circumvent androgen receptor (AR)-blockade and cell death. As standard AR-directed therapies fail to block the GR and GR inhibitors might result in unspecific side effects, the identification of GR signature genes, which are better suitable for a targeting approach, is of clinical importance. In a recent study, we therefore investigated the altered epithelial and stromal GR signature in PCa cells after GC treatment and identified monoamine oxidase A (MAO-A) as a mutual directly up-regulated epithelial and stromal GR target. MAO-A is a mitochondrial membrane-bound oxidoreductase that catalyzes the degradation of biogenic and xenobiotic amines. MAO-A is highly upregulated during PCa progression and after GC treatment. Pharmacological MAO-A inhibition may therefore amplify standard-of-care medication for patients with advanced PCa. Although these findings shed new light on this topic, past and current research has mainly focused on systemic GC effects in PCa patients as well as on epithelial GR signaling and its impact on tumor progression. However, little is known about direct GC-mediated effects on GR activity in the stromal tumor microenvironment (TME), which is even known to be significantly involved in tumor progression. Possible functional consequences on the stromal compartment itself and via paracrine effects on the prostate epithelium might influence tumor progression significantly. GC´s might be an additional yet unknown reason for developing therapy resistance. Findings gained in this ongoing study demonstrate that elevated stromal GR signaling after GC treatment is associated with altered levels of soluble factors and ECM re-modeling. The modified GC-treated stromal tumor micro-environment significantly influences epithelial tumor cell growth and must be considered in future therapeutic strategies.

Regulation of the AR splice variant V7 by small nucleotide variants (F.R. Santer, J. van Goubergen)

The androgen receptor (AR) splice variant V7 is frequently detected in castration resistant prostate cancer patients. Lacking the ligand binding domain it cannot be targeted by current endocrine treatments for prostate cancer and thus drives the progression of this disease. Compared to the full length isoform, ARV7 mRNA has a different 3´ untranslated region (3´UTR), suggesting that ARV7 is differently regulated at the post-transcriptional level. As a tool to investigate possible regulatory mechanisms of the 3´UTR on ARV7 mRNA expression and stability, we characterize the allelic effects of small nucleotide polymorphisms with high minor allele frequency. Since ARV7 expression is used as a therapy-guiding biomarker, these quantitative expression trait loci (eQTL) could be used to improve the specificity of this biomarker.

Improvement of diagnosis of homologous recombination deficiency by liquid biopsy for personalized medicine with PARP inhibitors (A. Pohl, F.R. Santer)

PARP inhibitors have been recently approved for the treatment of castration resistant prostate cancer, if patients present with somatic pathogenic mutations in BRCA1 or BRCA2 leading to homologous recombination deficiency (HRD) and genomic instability. However, the diagnosis of HRD in prostate cancer is frequently hampered by the non-availability of tumor specimen. To overcome this problem, we establish methods in this project to isolate genomic DNA from circulating tumor cells for HRD analysis using SNP arrays and targeted sequencing. An additional aspect of this project is to determine the pathogenicity of BRCA1/2 variants of uncertain significance by developing a diagnostic test for measuring HRD.

CDK12 inhibition in prostate and ovarian cancer (F. Santer)

It has been shown that CDK12 has a role in gene transcription by regulating the access to internal poly-adenylation sites, thus ensuring full length transcripts. Inhibition of CDK12 activity leads to decreased gene expression levels particularly affecting genes of DNA repair pathways thus inducing a homologous recombination deficiency-like phenotype. Here, we tested the anti-cancer effects of a CDK12 inhibitor on prostate and ovarian cancer cell lines alone, and in combination with a PARP inhibitor or a DNA-damaging chemotherapy.

Influence of vitamin D on testicular carcinogenesis (R. Pichler, G. Tulchiner, F.R. Santer)

Previously, we discovered a high seasonal incidence of testicular cancer, being highest during winter months. We therefore speculate, whether vitamin D, a known anti-cancer agent, could be involved in the carcinogenesis of testicular germ cell tumors. Interestingly, the vitamin D receptor gene signature is differentially expressed in seminomas vs. non-seminomas. Isochrome 12p formation is a genetic feature of almost all germ cell tumors, and this chromosome contains numerous genes of vitamin D metabolism. Therefore, this project intends to analyze the regulation of vitamin D metabolism in testicular cancer and its impact on carcinogenesis.

Tumor microenvironment and novel targets in prostate cancer (N. Sampson, E. Brunner, E. Damisch, L. Nommensen, L. Neumann)

The stromal tumor microenvironment (TME) plays a critical role in the development, progression and therapy response of prostate cancer. Cancer-associated fibroblasts (CAFs) are the dominant cell type within the PCa TME, but display considerable heterogeneity at both the molecular and functional level. We are investigating the molecular and physical mechanisms underlying CAF plasticity and their clinical relevance on disease progression and therapy efficacy with the aim of identifying new targets that may (i) enable the distinction between progressive vs. indolent disease and (ii) be exploited therapeutically in an adjuvant stromal-targeted approach. Additionally, we are investigating the role of NADPH oxidase 4 (NOX4), a ROS-producing enzyme that is expressed in a subpopulation of CAFs, which we previously showed to be a central mediator of a signaling hub at the tumor cell-CAF interface.

Novel biochemical targets and biomarkers in bladder cancer and renal cell carcinoma (R. Pichler, A. Lindner)

Platinum-based chemotherapy is the standard of care concerning first-line systemic therapy for metastatic disease in urothelial cancer. Resistance to chemotherapy despite an initial response is linked with the ability to remove platinum-based DNA adducts and to repair chemotherapy-induced DNA lesions by various DNA repair proteins. We recently detected a specific amplification on the chromosomal region 7p12 associated with non-response to neoadjuvant chemotherapy and, consequently, worse survival outcomes after radical cystectomy. When analyzing the sequence of interest in detail, 7p12.2–p11.2 prioritized genes that previously had not been reported as regulators of platinum-based chemotherapy responses in bladder cancer including HUS1. In order to define the possible importance of HUS1 in the regulation of cellular proliferation, parental and resistant cells were treated with increasing concentrations of either control or HUS1 siRNA. HUS1 protein expression was observed in both human basal urothelial cancer cell lines UM-UC-3 and HT1197. In cisplatin-sensitive cells, knock-down of HUS1 inhibited cellular proliferation in the presence of cisplatin. On the other hand, knock-down of HUS1 in resistant cells did not result in a re-sensitization to cisplatin. Thus, HUS1 may acts as an oncogene in UC and might be a key determinant of the cellular response to cisplatin-based chemotherapy
In RCC, we described novel therapeutic options for a rare, aggressive subtype of RCC, termed Fumarate hydratase (FH) – deficient renal cell carcinoma (FHdRCC) with a focus on anti-angiogenesis and EGFR-blockade. We also address potential targets that arise within the metabolic escape routes taken by FH-deficient cells for cell growth and survival. Moreover, we described the importance of c-Met inhibition for direct antitumor effects on proliferation, angiogenesis, and metastasis, and indirect antitumor effects via prevention of the induction of immunosuppressive mechanisms (PD-L1, TGFβ, IDO1). c-Met inhibition is key to overcome resistance to immune checkpoint inhibition and to maximize the efficacy of immunotherapy in RCC. Finally, CXCR3high cell density was associated with high T cell infiltration and advanced tumor stage, worsening recurrence-free survival in surgically resected RCC patients. In addition to its prognostic value, CXCR3 might be a predictive biomarker to further guide therapy decision for adjuvant (immuno)therapy in localized RCC.

Tumor immunology and immunotherapy (M. Thurnher, D. Klaver)

The Tumor Immunology Unit examines the diverse interactions between developing tumors and the immune system. We examine both, the favorable and adverse aspects of this crosstalk at various levels. This includes the study of tumor and immune cell metabolism as well as the investigation of chemokine-driven infiltration of the tumor tissue by immune cells. In attempts dedicated to the identification of biomarkers, we perform immune monitoring of approved cancer therapies. At the molecular level, we examine the role of the G protein coupled ATP receptor P2Y11 in human M2 macrophages. In these cells, the P2Y11 receptor translates the danger signal ATP into cytoprotective responses and may thus critically affect the efficacy of tumor immunotherapy.


Selected Publications

Team I. Heidegger

Heidegger I, Fotakis G, Offermann A, Goveia J, Daum S, Salcher S, Noureen A, Timmer-Bosscha H, Schäfer G, Walenkamp A, Perner S, Beatovic A, Moisse M, Plattner C, Krogsdam A, Haybaeck J, Sopper S, Thaler S, Keller MA, Klocker H, Trajanoski Z, Wolf D, Pircher A (2022): “Comprehensive characterization of the prostate tumor microenvironment identifies CXCR4/CXCL12 crosstalk as a novel antiangiogenic therapeutic target in prostate cancer”, Mol Cancer 21:132.

Kafka M, Burtscher T, Fritz J, Schmitz M, Bektic J, Ladurner M, Horninger W, Heidegger I (2022): “Real-world comparison of Docetaxel versus new hormonal agents in combination with androgen-deprivation therapy in metastatic hormone-sensitive prostate cancer descrying PSA Nadir <0.05 ng/ml as marker for treatment response”, World J Urol, 2022.

Schaefer G, Bednarova N, Heidenreich A, Klocker H, Heidegger I (2021): “KDM5D predicts response to docetaxel chemotherapy in metastatic castration resistant prostate cancer”, Transl Androl Urol 10:3946-3952.

Steuber T, Heidegger I, Kafka M, Roeder M, Chun F, Preisser F, Palisaar RJ, Hanske J, Budaeus L, Schiess R, Keller T, Semjonow A, Hammerer P, Manka L, Ecke T, Schwentner C, Ohlmann C (2022): “PROPOSe: a real-life prospective study of Proclarix, a novel blood-based test to support challenging biopsy decision-making in prostate cancer”, Eur Urol Oncol 5:321-327.

Team Z. Culig

Furlan T, Kirchmair A, Sampson N, Puhr M, Gruber M, Trajanoski Z, Santer FR, Parson W, Handle F, Culig Z (2021): “MYC-mediated ribosomal gene expression sensitizes enzalutamide-resistant prostate cancer cells to EP300/CREBBP inhibitors”, Am J Pathol 191:1094-1107.

Offermann A, Kang D, Watermann C, Weingart A, Hupe MC, Saraji A, Stegmann-Frehse J, Kruper R, Schüle R, Pantel K, Taubert H, Duensing S, Culig Z, Aigner A, Klapper W, Jonigk D, Kühnel MP, Merseburger AS, Kirfel J, Sailer V, Perner S (2021): “Analysis of tripartite motif (TRIM) family gene expression in prostate cancer bone metastases”, Carcinogenesis 42:1475-1484.

Vakhrusheva O, Erb HHH, Bräunig V, Markowitsch SD, Schupp P, Baer PC, Slade KS, Thomas A, Tsaur I, Puhr M, Culig Z, Cinati Jr. J, Michaelis M, Efferth T, Haferkamp A, Jüngel E (2022): “Artesunate inhibits the growth behavior of docetaxel-resistant prostate cancer cells”, Front Oncol 12:789284.

Muresan X, Slabakova E, Prochazkova J, Drapela S, Fedr R, Pickova M, Vacek O, Vichova R, Suchankova T, Bouchal J, Kurfurstova D, Kral M, Hulinova T, Sykora RP, Student V, Hejret V, van Weerden WM, Puhr M, Pustka V, Potesil D, Zdrahal Z, Culig Z, Soucek K (2022): “Toll-like receptor 3 overexpression induces invasion of prostate cancer cells, whereas its activation triggers apoptosis”, Am J Pathol 192:1321-1335.

Limberger T, Schlederer M, Trachtova K, Garces de los Fayos Alonso I, Yang J, Högler S, Sternberg C, Bystry V, Oppelt J, Tichy B, Schmeidl M, Kodajova P, Jäger A, Neubauer HA, Oberhuber M, Schmalzbauer MS, Pospisilova S, Dolznig H, Wadsak W, Culig Z, Turner SD, Egger G, Lagger S, Kenner L (2022): “KMT2C methyltransferase domain regulated INK4A expression suppresses prostate cancer metastasis”, Mol Cancer 21:89.

Team I. Eder-Neuwirt

Ladurner M, Wieser M, Eigentler M, Seewald M, Dobler G, Neuwirt H, Kafka M, Heidegger I, Horninger W, Bektic J, Klocker H, Obrist P, Eder IE (2021): “Validation of cell-free RNA and circulating tumor cells for molecular marker analysis in metastatic prostate cancer”, Biomedicines 9:1004.

Kafka M, Gruber R, Neuwirt H, Ladurner M, Eder IE (2022): “Long-term treatment with simvastatin leads to reduced migration capacity of prostate cancer cells”, Biomedicines 11:29.

Team M. Puhr

Keresztes D, Csizmarik A, Nagy N, Modos O, Fazekas T, Bracht T, Sitek B, Witzke K, Puhr M, Sevcenco S, Kramer G, Shariat S, Kuronya Z, Takacs L, Tornyi L, Lazar J, Hadaschik B, Laszik A, Szucs M, Nyiradi P, Szarvas T (2022): “Comparative proteome analysis identified CD44 as a possible serum marker for docetaxel resistance in castration-resistant prostate cancer”, J Cell Mol Med 26:1332-1337.

Kalogirou C, Linxweiler J, Schmucker P, Snaebjornsson MT, Schmit W, Wach S, Krebs M, Hartmann E, Puhr M, Müller A, Spahn M, Seitz AK, Frank T, Marouf H, Büchel G, Eckstein M, Kübler H, Eilers M, Saar M, Junker K, Röhrig F, Kneitz B, Rosenfeldt MT, Schulze A (2021): “MiR-205-driven downregulation of cholesterol biosynthesis through SQLE-inhibition identifies therapeutic vulnerability in aggressive prostate cancer”, Nat Commun 12:5066.

Puhr M, Eigentler A, Handle F, Hackl H, Ploner C, Heidegger I, Schaeffer G, Brandt MP, Hoefer J, van der Pluijm G, Klocker H (2021): “Targeting the glucocorticoid receptor signature gene Mono Amine Oxidase-A enhances the efficacy of chemo- and anti-androgen therapy in advanced prostate cancer”, Oncogene 40:3087-3100.

Pardella E, Pranzini E, Nesi I, Parri M, Spatafora P, Torre E, Muccilli A, Castiglione F, Fambrini M, Sorbi F, Cirri P, Caselli A, Puhr M, Klocker H, Serni S, Raugei G, Magherini F, Taddei M (2022): “Therapy-induced stromal senescence promoting aggressiveness of prostate and ovarian cancer”, Cells 11:4026.

Beier AK, Puhr M, Stope MB, Thomas C, Erb HHH (2022): “Metabolic changes during prostate cancer development and progression”, J Cancer Res Clin Oncol, in press.

Csizmarik A, Keresztes D, Nagy N, Bracht T, Sitek B, Witzke K, Puhr M, Tornyi I, Lazar J, Takacs L, Kramer G, Sevcenco S, Maj-Hes A, Juranyi Z, Hadaschik B, Nyirady P, Szarvas T (2022): “Proteome profiling of enzalutamide-resistant cell lines and serum analysis identified ALCAM as marker of resistance in castration-resistant prostate cancer”, Int J Cancer 151:1405-1419.

Team N. Sampson

Kang J, La Manna F, Bonollo F, Sampson N, Alberts I L, Mingels C, Afshar-Oromieh A, Thalmann GN, Karkampouna S (2022): “Tumor microenvironment mechanisms and bone metastatic disease progression of prostate cancer”, Cancer Lett 530:156-169.

Team R. Pichler

Lindner AK, Furlan T, Orme JJ, Tulchiner G, Staudacher N, D’Andrea D, Culig Z, Pichler R (2022): „HUS1 as a Potential Therapeutic Target in Urothelial Cancer“, J Clin Med 11:2208.

Lindner AK, Tulchiner G, Seeber A, Siska PJ, Thurnher M, Pichler R (2022): „Targeting strategies in the treatment of fumarate hydratase deficient renal cell carcinoma“, Front Oncol 12:906014.

Lindner AK, Pichler M, Thurnher M, Pichler R (2022): „Targeting c-Met to Improve Immune Checkpoint Inhibition in Metastatic Renal Cell Carcinoma“, Eur Urol 81:1-2.

Tulchiner G, Pichler R, Ulmer H, Staudacher N, Lindner AK, Brunner A, Zelger B, Steinkohl F, Aigner F, Horninger W, Thurnher M (2021): “Sex-specific hormone changes during immunotherapy and its influence on survival in metastatic renal cell carcinoma”, Cancer Immunol Immunother 70:2805-2817.

Pichler R, Lindner AK, Schäfer G, Tulchiner G, Staudacher N, Mayr M, Comperat E, Orme JJ, Schachtner G, Thurnher M (2021): “Expression of ADAM Proteases in Bladder Cancer Patients with BCG Failure: A Pilot Study”, J Clin Med 10:764.

Tulchiner G, Brunner A, Schmidinger M, Staudacher N, Orme JJ, Thurnher M, Horninger W, Culig Z, Pichler R (2021): “CMTM6 expression as a potential biomarker for immunotherapy in metastatic renal cell carcinoma”, BJU Int 128:29-132.

Lindner AK, Schachtner G, Tulchiner G, Thurnher M, Untergasser G, Obrist P, Pipp I, Steinkohl F, Horninger W, Culig Z, Pichler R (2021): „Lynch Syndrome: Its Impact on Urothelial Carcinoma“, Int J Mol Sci 22:531.

Team M. Thurnher

Gruenbacher G, Gander H, Dobler G, Rahm A, Klaver D, Thurnher M (2021): “The human G protein-coupled ATP receptor P2Y11 is a target for anti-inflammatory strategies”, Br J Pharmacol 178:1541-1555.

Klaver D, Thurnher M (2021): “Control of Macrophage Inflammation by P2Y Purinergic Receptors”, Cells 10:1098.

Klaver D, Gander H, Dobler G, Rahm A, Thurnher M (2022): “The P2Y11 receptor of human M2 macrophages activates canonical and IL-1 receptor signaling to translate the extracellular danger signal ATP into anti-inflammatory and pro-angiogenic responses”, Cell Mol Life Sci 79:519.

Selection of Funding

Zoran Culig: Euregio: “Roles and targeting of RIOK1 in resistant prostate cancer”

Zoran Culig: DFG FWF International Project: “microRNA and regulation of MED in prostate cancer”

Zoran Culig: Eureka FFG Project: “ReDIRECt – a new application for drugs for urothelial cancer under consideration of molecular results”

Martin Puhr, Austrian National Bank Project: “The impact of glucocorticoid administration on prostate cancer progression”

Frédéric R. Santer: Fondation Cancer Luxembourg: “Androgen receptor splice variant AR-V7 in advanced prostate cancer. Improvement of biomarker specificity through identification of single nucleotide polymorphisms”

Frédéric R. Santer: Astra Zeneca Austria (for studies on PARP inhibitors)

Natalie Sampson: International Joint Project, Austrian Science Fund and Swiss National Fund: “Therapy resistance in prostate cancer: role of tumor stroma heterogeneity”

Natalie Sampson: Stand Alone Project, Austrian Science Fund: “Functional significance of NADPH oxidase 4 in the prostate cancer stromal tumor microenvironment”

Martin Thurnher: Austrian Science Fund: “The ATP receptor P2Y11 engages nonapoptotic functions of Fas”


Lukas Kenner, Department of Pathology, Medical University of Vienna

Karel Soucek, Institute for Biophysics, Brno

Sven Perner, Department of Pathology, University Clinic Schleswig Holstein, Lübeck

Eva Jüngel and Maximilian Brandt, Department of Urology, University Clinic Mainz

Maria Frantzi, Mosaiques Diagnostics, Hannover

Peter deWulf, University of Trento

Helge Taubert, University Clinic Erlangen

Achim Aigner, University of Leipzig

Gabri van der Pluijm, Ledien University Medical Center

Marialetizia Taddei, University of Florence

Holger Erb, University Clinic Dresden

Marcus V. Cronauer, University Clinic Bonn

Marianna Kruithof-de Julio, Department for BioMedical Research, Urology Research Laboratory, University of Bern

Congress organization: Annual meeting European Section of Urological Research, Innsbruck October 2022 (Chair: Isabel Heidegger)