Experimental Hepatology, Inflammation and Cancer

Junior Research Group Experimental Hepatology, Inflammation and Cancer

Dr. Dr. Michael Dill

Microscopy image of a hepatocyte organoid
© dkfz.de

Tumors consist of cancer cells and a multitude of other cell types that, through complex interactions, successfully create a tumor microenvironment (TME) that sustains cancer growth and assists in immune evasion. The recent success story of successful treatment by immune check point inhibitors in some cancer types illustrates the importance of anti-tumor immunity. However, the response rate on these therapeutics is very individual and dependent on the composition and activity of the cells in the TME. There is growing evidence that not only classic immunogenic factors, such as the mutational burden of cancer cells, define the anti-tumor immune response but that also oncogenic signaling pathways might play an important role in various ways through mechanisms not thoroughly understood yet.
Our lab investigates how different oncogenic signaling pathways each directly influence the TME and thus anti-tumor immunity. We focus primarily on liver cancer, which is characterized by a substantially genetic and morphologic heterogeneity and therefore particularly interesting to study. We use novel organoid-based preclinical liver cancer models that allow us to rebuild this genetic diversity and to study liver cancer in an immunologically intact setting. With single cell analyses we perform careful characterizations of the molecular cell-cell interactions and utilize functional genomic technologies to further probe their relevance. These models are complemented with organoid systems cultivated from human material.

The aim of our research is the classification of cancer genome – TME phenotype correlation patterns, the identification of immunotherapy resistance mechanisms specific to various oncogenic signaling pathways, and the discovery of therapeutically targetable pathway components of immune evasion, to formulate tumor-specific synergistic therapeutical approaches as a personalized treatment strategy.


Dr. Dr. Michael Dill
Experimental Hepatology, Inflammation and Cancer (F240)
Deutsches Krebsforschungszentrum
Im Neuenheimer Feld 242
69120 Heidelberg
Tel: +49 (0)6221 42-1520

Selected Publications

  • Pepe-Mooney B.J.*, Dill M.T.*, Alemany A., Ordovas-Montanes J., Matsushita Y., Rao A., Sen A., Miyazaki M., Anakk S., Dawson P.A., Ono N., Shalek A.K., van Oudenaarden A., Camargo F.D. (2019). Single-cell analysis of the liver epithelium reveals dynamic heterogeneity and an essential role for YAP in homeostasis and regeneration. Cell Stem Cell., 25(1):23-38.
  • Dill M.T., Makowska Z., Trincucci G., Gruber A.J., Vogt J.E., Filipowicz M., Calabrese D., Krol I., Lau D.T., Terracciano L., van Nimwegen E., Roth V., Heim M.H. (2014). Pegylated IFN-? regulates hepatic gene expression through transient Jak/STAT activation. J Clin Invest., 124(4):1568-81
  • Dill M.T., Tornillo L., Fritzius T., Terracciano L., Semela D., Bettler B., Heim M.H., Tchorz J.S. (2013). Constitutive Notch2 signaling induces hepatic tumors in mice. Hepatology. 57(4):1607-19
  • Dill M.T.*, Rothweiler S.*, Djonov V., Hlushchuk R., Tornillo L., Terracciano L., Radtke F., Heim M.H., Semela D. (2012). Disruption of Notch1 induces vascular remodeling, intussusceptive angiogenesis and angiosarcomas in livers of mice. Gastroenterology., 142(4):967-977
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