Hämatologie

Using preclinical models as well as innovative co-culture experiments and human tissue and blood samples, we aim to elucidate how malignant lymphoma cells shape their tumor microenvironment to receive important growth signals and to regulate or inhibit immune cell responses.

In addition, we will identify genetic alterations and their impact on the pathogenesis and tumor microenvironment of lymphoid neoplasms.

Contact

Alexander Deutsch  
T: +43 316 385 72816
Forschung

Our Focus

  • Tumormicroenvironment in Lymphoma
  • The Role of the NR4A nuclear orphan Receptor Family in Lymphomagenesis

Projects

The tumor suppressive role of NR4A1 in aggressive lymphomas

  • Duration: 2021-2025
  • Funded by: MEFOgraz

NR4A1-mediated regulation of immune evasion in lymphoma

  • Tumour cells have developed a number of mechanisms to avoid or suppress their recognition, targeting and killing by immune cells. We found out that a part of aggressive B cell lymphomas, a tumour consisting of the antibody-producing cells, exhibited low expression of the transcription factor NR4A1. NR4A1, like other transcription factors, regulates numerous biological processes in cells. However, its function has not been yet investigated in aggressive B cell lymphomas.
  • Duration: 2023-2026
  • Funded by: FWF

NR4a1-P53 axis in the immune evasion of aggressive lymphomas

  • Aggressive lymphomas are among the most common types of lymphoid cancers and consist of Burkitt’s lymphoma, diffuse large B cell lymphoma (DLBCL), follicular lymphoma grade 3. While checkpoint blockade therapies (CBTs) have emerged as a promising avenue to counteract tumor evasion, this treatment form comes with substantial cost burdens and often rely on trial-and-error approaches. Importantly, only a small percentage of lymphoma patients (10-20%) respond favorably to CBT, partly due to the limited understanding of the regulation of immune checkpoints during lymphoma development and the absence of predictive biomarkers. Our recent investigations have shed light on key factors contributing to poor outcomes in patients with DLBCL. We observed significant decreases in the levels of NR4A1 and p53, which are important regulators of gene expression and known tumor suppressors, alongside high expression of checkpoint components.
  • Duration: 2024-2029
  • Funded by: FWF

Team

Cooperations

  • Alan Ramsay, Comprehensive Cancer Centre, King’s College, London, UK
  • Monika Brunner-Weinzierl, Department of experimental pediatrics, Otto-von-Guericke-University, Magdeburg, Germany
  • Akihiko Yoshimura, Department of Microbiology and Immunology, Keio University, Japan
  • Georg Stary, Ludwig Boltzmann Institute for Rare and Undiagnosed Diseases, Department of Dermatology, Medical University of Vienna
Forschungsteam Deutsch