Dr. Melek Canan Arkan

T: +4969-63395-600
Email: Arkan@med.uni-frankfurt.de

Dr. Ursula Dietrich

T: +4969-63395-216
Email: Ursula.Dietrich@gsh.uni-frankfurt.de



Dr. Henner Farin

T: +49 69 63395-520
Email: Farin@gsh.uni-frankfurt.de




Prof. Dr. Florian Greten

T: +4969-63395-232
Email: Greten@gsh.uni-frankfurt.de




Prof. Dr. Daniela Krause

T: +4969-63395-500
Email: Krause@gsh.uni-frankfurt.de



Dr. Hind Medyouf

T: +4969-63395-540
Email: Medyouf@gsh.uni-frankfurt.de




Dr. Lisa Sevenich

T: +4969-63395-560
Email: Sevenich@gsh.uni-frankfurt.de




Prof. Dr. Winfried Wels

T: +4969-63395-188
Email: Wels@gsh.uni-frankfurt.de

  • Diet-induced obesity is a major risk factor for the development of cancer. Although alterations in inflammatory and bioenergetic pathways are critical in linking excessive weight gain to cancer, there is now sufficient evidence to also suggest disease progression may indeed have more to do with the diet itself than increased obesity per se. The diet is shaped by multiple diverse factors such as culture, nutritional knowledge, price, availability, taste and convenience. With our current knowledge on the importance of the reciprocal interaction between host and environmental factors in selecting a microbiota that favours carcinogenesis, the food consumption is critical. More...

  • Our research priority is the identification and characterization of virus neutralizing antibodies and their epitopes. Using different techniques like phage display and direct antigen-specific B cell sorting we identify these antibodies as well as the epitopes they target on the viral envelope glycoproteins as basis for vaccine development. We also develop new HIV-1 Env immunogens mimicking native epitopes as antigens and immunogens as well as for structural analysis. I a further project we analyze the infectivity of human hematopoietic stem cells (HSC) and multipotent progenitors (MPP) by HIV-1 in order to further elucidate the role of this compartment as HIV-1 reservoir. More...

  • Our lab explores the 3D ‘organoid’ culture system as a model for tumors derived from the gastrointestinal epithelium. The system allows to expand primary intestinal stem cells under full control of the exogenous ‘microenvironment’. Exposure to signals such as inflammatory cytokines, growth factors, microbial and metabolic cues are analyzed to dissect tumorspecific vulnerabilities. Our goal is to understand how tumor cells respond to microenvironmental signals, as a step towards patient-specific therapies.

  • Our research interest focuses on signal transduction pathways in different cell types of the tumor microenvironment using conditional knockout technology. Inflammation is a strong trigger of cell plasticity, particularly in recruited immune cells such as T cells and myeloid cells. However, plasticity of tumor cells plays also a very important role during invasion and metastasis especially in terms of epithelial-mesenchymal transition (EMT). Over the last years we have been specifically addressing how the inflammatory tumor microenvironment affects cell plasticity in mouse models of colorectal cancer.

  • Traditionally, treatment of the leukaemias has targeted the leukaemia cells themselves. However, several groups, including ours, have shown that pharmacological modification of the bone marrow microenvironment, which „houses“ the leukaemia, can lead to eradication of leukaemic stem cells. By the use of various leukaemia models and pharmacological agents our laboratory focuses on inhibiting different pathways of communication between leukaemia cells and the bone marrow niche in order to improve current therapies.

  • Hematologic malignancies are complex diseases in which interactions between neoplastic cells and components of the bone marrow microenvironment play a pivotal role in disease pathogenesis. Our group aims to decipher the cellular and molecular events at play in the bone marrow of patients with myelodysplastic syndromes and related myeloid malignancies, with a particular emphasis on the cross-talk between niche cells and their hematopoietic counterparts. We use relevant model systems, including unique patient-derived xenografts, to evaluate the possibility to target diseased cells through their niche support and subsequently pave the way to preclinical studies aiming at improving the outcome for patients.

  • The tumor microenvironment is a critical mediator of disease progression in brain metastasis. Detailed knowledge of the cellular and molecular mechanisms that drive brain metastasis is essential to provide better treatment options for brain metastases patients. Our research goal is to dissect the complex interactions between tumor cells from different primary tumor entities (melanoma, breast- and lung cancer) and brain resident- as well as recruited inflammatory cells during different stages of cerebral colonization and to understand the effects of standard of care therapy on the brain metastasis microenvironemt. We seek to translate our findings into clinical application for the development of targeted- or immune therapies against brain metastases. More ...

  • Aim of our work is the development of effective immunotherapies for the treatment of cancer. Our main focus are natural killer (NK) cells, which are part of the innate immune system and play an important role in the defense against viral infections and malignant cells. By expression of so-called chimeric antigen receptors (CARs) in NK cells and other cytotoxic lymphocytes, we generate genetically modified variants that selectively recognize tumor cells by CAR-mediated binding to tumor-associated cell surface antigens. This triggers effector cell activation and target cell lysis.



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