Using cell and molecular biology techniques, high-throughput approaches as well as in vivo mouse models, we aim to gain insight into the network of oncogenic defects in transformed B and T cells.
In particular, we are interested in the link between deregulated signaling and transcription factor activities, disruption of cellular differentiation and oncogenic transformation. Using primarily classical Hodgkin lymphoma (HL) and anaplastic large cell lymphoma (ALCL) as model systems, we analyze the role of lineage infidelity, cellular reprogramming and activation of lineage-inappropriate survival signals in lymphomagenesis, as exemplified by our work on the transcription factor E2A, which is essential for the development of B and T lymphoid cells, or aberrant expression of CSF1R, a myeloid-specific growth and survival factor, in lymphoid malignancies.
In addition to studying lymphoma cell autonomous processes, we focus on the elucidation of lymphoma - stroma interactions. Along these lines, we are dissecting signaling networks by chemokines and cytokines that provide essential growth and survival signals for B cell lymphomas. Collectively, our work does not only address fundamental aspects of leukemia and lymphoma pathogenesis, but also aims at providing therapeutic solutions.