Research Focus
Prof. Lukas Kenner's research is centered on the molecular mechanisms driving cancer progression, particularly in prostate carcinoma (PCa) and anaplastic large cell lymphoma (ALCL). His work integrates patient-derived samples with advanced in vitro and in vivo model systems, including transgenic mouse models, to explore how hormonal, genetic, and environmental factors contribute to cancer development and metastasis.
In prostate cancer (PCa), Kenner's team investigates critical pathways such as JAK/STAT signaling (e.g., Pencik et al., 2015) and epigenetic regulation (Limberger et al., 2022), as well as the impact of hormonal regulation (Aksoy et al., 2020) on tumor aggressiveness. His research has uncovered new biomarkers and therapeutic targets for aggressive PCa (e.g., Oberhuber et al., 2020), and employing bioinformatics and AI to analyze complex data from PCa PET-CT/MRI imaging and clinical data, human tissue samples and transgenic model systems (e.g. Ning et al., 2024).
In anaplastic large cell lymphoma (ALCL), Kenner has demonstrated the significance of PDGFRβ in tumor survival (Laimer et al., 2012) and recently identified STAT5 as a druggable target downstream of PDGFRβ (Garces et al., 2022). His research in ALCL provides critical insights into targeted therapies for this highly malignant T-cell lymphoma.
A major emerging focus in Kenner's research is the role of micro- and nanoplastics (MNPs) in cancer. His recent studies (Gruber et al., 2022; Kopatz et al., 2023) show that MNPs can promote cancer progression by altering cell migration (Brynzak-Schreiber et al., 2024) and drug efficacy (Dick et al., 2024), as well as breaching biological barriers such as the blood-brain barrier (Kopatz et al., 2023). This work is part of a €4 million funded project (microOne) that investigates MNPs as environmental carcinogens, specifically exploring their potential role in colorectal and prostate cancer.
Main Objectives
Kenner's lab aims to identify novel molecular drivers of cancer initiation, progression, and metastasis, with a particular focus on:
- Hormonal regulation and metabolic reprogramming in PCa.
- The JAK/STAT and PDGFRβ/STAT5 pathways in ALCL.
- The carcinogenic potential of MNPs, including their role in inducing genetic mutations and therapy resistance in cancer.
The research seeks to translate these findings into therapeutic strategies and biomarkers that can enhance cancer diagnosis, treatment, and patient outcomes.
Approach
The laboratory employs an integrated approach, combining genomics, transcriptomics, and proteomics with advanced imaging techniques and AI-based data analysis. Candidate genes and pathways are validated through functional assays in in vitro and murine xenograft models. A key focus is correlating molecular findings with clinical outcomes, enabling the identification of biomarkers that can inform personalized treatment strategies. Kenner's recent work on MNPs introduces a new dimension to cancer research by studying the interaction between environmental toxins and cancer biology, a field that is still in its infancy but has significant implications for public health.
2021-2025 microOne 'Microplastics, a hazard to human health',
4 years, Role of L. Kenner: Proposer, writer, and scientific lead. Budget: 4 Mill EUR.
microONE is a research project with a specific focus on the health effects of micro- and nanoplastic particles on human health, which is currently funded as a COMET module by the Austrian Research Promotion Agency (FFG). microONE is THE reference project within the "Action Plan Microplastics 2022-2025" of the Federal Ministry for Climate Protection, Environment, Energy, Mobility, Innovation and Technology in Austria. https://www.cbmed.at/project/microone/
2018-2025 Christian Doppler Laboratory for Applied metabolomics (CDL-AM)
4 years, Role of L. Kenner: Proposer, writer, and scientific director. Budget: 2,8 Mill EUR. The CDL-AM advances personalized treatment and therapy monitoring of cancer patients by using PET imaging, whole exome sequencing, and patient outcome data with machine learning to characterize non-invasively.
2020-2025 WWTF Deciphering breast cancer heterogeneity and tumor microenvironment with correlative imaging
5 years, Role of L. Kenner: Co-proposer and writer and Co-PI. Budget: 700.000.- EUR. Member of the consortium together with Katja Pinker (Columbia University, NY) and Goran Medulovic (MUW). This project aims to combine advanced imaging (PET/MRI) with molecular profiling techniques linked by AI to better identify aggressive tumors and reduce invasive procedures, ultimately advancing personalized breast cancer therapy. https://www.wwtf.at/funding/programmes/ls/LS19-018/
2024-2027 Horizon-MSCA-DN eRaDicate
3 years, Role of L. Kenner: Co-proposer, Co-writer, and member of the consortium. This research explores new combination therapies for advanced PCa by targeting the TRβ/AR/RARγ/VDR axis and cancer stem cells, evaluating anti-thyroid and nuclear receptor agents, and validating findings in models and patient data. https://www.eradicate-project.eu
2023-2026 Horizon-MSCA-DN FANTOM
3 years, Role of L. Kenner: Co-proposer, Co-writer, and member of the consortium. The research program focuses on ALCL using advanced model systems and multi-omics technologies to study its biology. The goal is to develop non-invasive biomarkers and new therapies, leading to clinical trials addressing chemotherapy toxicity, over-treatment, and drug resistance. https://fantom-project.eu/about/
2021-2025 COST Action CA20101: "Plastics Monitoring Detection Remediation Recovery (PRIORITY)"
4 years, Role of L. Kenner: partner. A multidisciplinary science and technology research network aimed at developing, implementing, and consolidating strategies to address the global challenges of micro- and nanoplastics in the environment.
2024-2028 FWF 37116 Thyroid Hormone Receptor ß / AR Interplay in Prostate Cancer
4 years, Role of L. Kenner: Co-proposer, Co-writer, and associate partner. This research explores the role of thyroid hormone receptor β (TRβ) in promoting prostate cancer (PCa) growth and its interaction with the androgen receptor (AR). It aims to target the TRβ/AR axis for new therapies in castration-resistant PCa (CRPCa) and improve prognosis and treatment strategies.
2022-2025 FWF 34781 Role of TCR signalling in the genesis of ALCL
3 years, Role of L. Kenner: Proposer and writer. ALCL rarely expresses T-cell receptors and may develop through two pathways: one involving chronic TCR stimulation or inflammation-driven. The cancer cells mimic Th17 cells, linked to inflammation, and express the aryl hydrocarbon receptor (AHR), which may cause genetic damage and promote cancer. Research is focused on understanding these mechanisms to identify new therapies.
Univ.-Prof. Dr. Lukas KENNER
E-Mail: lukas.kenner@meduniwien.ac.at
» ORCID