Sophie Domhan, MDCenter of Cancer Systems Biology
Caritas St.Elizabeth's Medical Center
Tufts University School of Medicine
736 Cambridge Street
Boston, MA 02135
Tel: 617.779.6569
Mail: sophie.domhan [at] tufts.edu
Education and Training:
2003 MD, University of Heidelberg Medical School, Heidelberg, Germany
2003 Medical Thesis (Dr. med.), Topic: "The Role of CD95-Receptor/Ligand System in Acetylsalicylacid (Asprin) and Helicobacter pylori induced Apoptosis in Gastric Cancer Cells"
2004- Resident, Internal Medicine, Department of Nephrology, University of Heidelberg Medical School, Heidelberg, Germany
March 2008 - Research Associate, Department of Medicine, Center of Cancer Systems Biology, Caritas St. Elisabeth's Medical Center, Tufts University, Boston MA
Fellowships:
2003/04 Research Fellow: "Tumor Angiogenesis and Apoptosis", Department of Radiation Oncology, German Cancer Research Center (DKFZ)
2004- Research Associate: "Anti-angiogenic effects of novel immuosuppressive agents", Department of Nephrology, University of Heidelberg Medical School and Department of Radiation Oncology, German Cancer Research Center (DKFZ)
Research interests:
Anti-tumor effects of novel immunosuppressive drugs in transplantation medicine and prevention of post-transplant malignancies
Organ transplantation is a well established method for the therapy of end stage organ failure. With the increased life expectancy of allograft recipients post-transplant malignancy has emerged as an important cause for mortality in these patients. The tremendous growth of knowledge in cancer biology and the molecular mechanisms underlying anti-neoplastic effects of immunosuppressive agents offer new possibilities to address this issue. In our group we investigate potnetial anti-tumor and anti-angiogenic effects of novel targeted immunosuppressive agents.
Epithelial to mesenchymal transition in kidney fibrosis and tumor progression
Progression of chronic renal disease is considered to be an irreversible process that eventually leads to end-stage renal failure characterized by tissue fibrosis. Epithelial-to-mesenchymal transition (EMT) of injured epithelial cells plays an important role in the progression of fibrosis in the kidney. Several cellular and molecular mediators seem to be involved in this process. Possible targets for therapeutic intervention have been recently identified and may slow down or even reverse renal scar formation.
Most solid tumors are epithelial in origin. A loss of epithelial cell-markers and gain of mesenchymal cell-markers has been observed in patient tumor samples, particularly at the leading edge or invasive front of solid tumors and is associated with the degree of tumor progression. The interest of our group is to identify genes that contribute to EMT which might lead to new therapeutic strategies to prevent or even reverse this process.
Recent publications: