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Junior Research Group Adaptive Immunity and Lymphoma

Sandrine Sander, MD, PhD

A wide spectrum of methods is used to characterize and understand the GC reaction and GC B cell derived tumorigenesis.
© dkfz.de

Our immune system is essential for combating of pathogens, however, it may be the origin for diseases including malignancies. B cells are important players in adaptive immunity and our group is interested in B cell development and function as well as their malignant transformation in lymphoma cells. The focus of our research is the germinal center (GC) reaction which is important for antibody-mediated pathogen defense and origin of most human lymphoma entities.
GCs form after antigen contact in secondary lymphoid organs and host a variety of different immune cells. In these transient structures B cells modify their B cell receptor (BCR) encoding genes in order to produce high-affinity antibodies against the causative pathogen. During this process oncogenes and tumor suppressor gene are targeted accidentally by the DNA mutation machinery thereby promoting the transformation of B cells to lymphoma cells.

The Max Eder Research Group "Adaptive Immunity and Lymphoma" investigates cellular and molecular mechanisms underlying the GC reaction and lymphoma development. Based on this knowledge we aim to improve the treatment of lymphoma patients as well as to identify new approaches to enhance immune responses (e.g. in the context of vaccinations). With the help of innovative in vivo models that are characterized by selective targeting of genetic mutations in the cells of tumor origin, we are able to recapitulate human lymphomagenesis. These mouse models and state-of-the-art techniques in cancer biology and immunology will allow us to characterize tumor-specific aberrations and understand the transition from normal to malignant B cells.
In particular, our research aims to
(I) identify disease relevant genes and pathways in lymphoma pathogenesis based on the analysis of established in vivo and in vitro models. Based on strong collaborations with clinical partners our results are verified in human tumor samples as well as clinical observations are explored mechanistically in our animal models.
(II) analyze GC B cell and lymphoma cell interactions with immune cells and the effect of this crosstalk on tumor growth.
(III) decipher B cell receptor-mediated signaling as key pathway for B cell and lymphoma cell survival and function.
(IV) develop new pre-clinical lymphoma models.

Contact

Sandrine Sander, MD, PhD

Adaptive Immunity and Lymphoma (D180)

Deutsches Krebsforschungszentrum

Im Neuenheimer Feld 280

69120 Heidelberg

Tel: +49 (0)6221-421730

Fax: +49 (0)6221-421733
E-Mail: sandrine.sander@nct-heidelberg.de

Selected Publications

Sander S, Calado DP, Srinivasan L, Köchert K, Zhang B, Rosolowski M, Rodig SJ, Holzmann K, Stilgenbauer S, Siebert R, Bullinger L, Rajewsky K. (2012). Synergy between PI3K signalling and MYC in Burkitt lymphomagenesis. Cancer Cell, 22(2),167-179.
Sander S, Chu VT, Yasuda T, Franklin A, Graf R, Calado DP, Li S, Imami K, Selbach M, Di Virgilio M, Bullinger L, Rajewsky K. (2015). PI3 Kinase and FOXO1 transcription factor activity differentially control B cells in the germinal center light and dark zones. Immunity,43(6),1075-86.
Kabrani E, Chu VT, Tasouri E, Sommermann T, Baßler K, Ulas T, Zenz T, Bullinger L, Schultze J, Rajewsky K, Sander S (2018). Nuclear FOXO1 promotes lymphomagenesis in germinal center B cells. Blood, 132(25):2670-83.
Graf R, Seagal J, Otipoby K, Lam KP, Ayoub S, Zhang B, Sander S, Chu VT, Rajewsky K (2019). BCR dependent lineage plasticity in mature B cells. Science, 363: 748-53.