Hahn, Heidi, Prof. Dr.
Professor of Molecular Developmental Genetics
- Dr. med., University of Würzburg, 1992
- Postdoctoral Fellow, National Institutes of Health, Bethesda, Maryland, USA (1993 -1998)
- Junior Group Leader (BioFuture), Technical University of Munich (1999 - 2000)
- Professor of Molecular Developmental Genetics, University of Göttingen since 2001
Major Research Interests
Cancer is a disease that results from inappropriate cell division induced by hyperproliferation. In many cases, the development of cancer is associated with genes or signaling pathways important for patterning during embryogenesis.
We investigate the role of the Hedgehog/Patched (Hh/Ptch) signaling cascade in the development of solid tumors. The focus is on tumors caused by mutations in Ptch, such as medulloblastoma, rhabdomyosarcoma and basal cell carcinoma.
The first aim is the discovery of molecular and cellular events that trigger the initiation of Ptch associated tumors. The second aim is to elucidate the function of Hh/Ptch signaling during tumor progression. The current focus is on the interaction between Hh/Ptch and Wnt signaling during formation, progression and regression of basal cell carcinoma. In addition, we are investigating the role of Hh/Ptch signalling in myeloid or T cells during tumorigenesis. The third goal is the identification of drugs that target solid tumors caused by mutations in Ptch. Currently we are analyzing the anti-tumoral effects of the cytostatic drug doxorubicin and of Vitamin D3 derivatives. To test the anti-tumor activity of the drugs we use tumor-bearing Ptch mutant mice.
Homepage Department/Research Group
Selected Recent Publications
- Uhmann A; Heß I; Frommhold A; König S; Zabel S; Nitzki F; Dittmann K; Lühder F; Christiansen H; Reifenberger J; Schulz-Schaeffer W; Hahn H (2014). DMBA/TPA treatment is necessary for BCC formation from Patched deficient epidermal cells in Ptchflox/floxCD4Cre+/- mice. J Invest Dermatol. March 24
- Pelczar P; Zibat Z; van Dop WA; Heijmans J; Bleckmann A; Gruber W; Nitzki F; Uhmann A; Guijarro MV; Hernando E; Dittmann K; Wienands J; Dressel R; Wojnowski L; Binder C; Taguchi T; Beissbarth T; Hogendoorn PCW; Antonescu CR; Rubin BP; Schulz-Schaeffer W; Aberger F; van den Brink GR; Hahn H (2013). Inactivation of patched1 in mice leads to development of gastrointestinal stromal-like tumors that express pdgfr? but not kit. Gastroenterology 144(1): 134 -144.e6
- Nitzki F, Zibat A, Frommhold A, Schneider A, Schulz-Schaeffer W, Braun T, Hahn H (2011) Uncommitted precursor cells might contribute to increased incidence of embryonal rhabdomyosarcoma in heterozygous Patched1 mutant mice. Oncogene 30: 4428-36
- Nitzki F, Zibat A, König S, Wijgerde M, Rosenberger A, Brembeck F, Carstens PO, Frommhold A, Uhmann A, Klingler S, Reifenberger J, Pukrop T, Aberger F, Schulz-Schaeffer W, Hahn H (2010) Tumor stroma-derived Wnt5a induces differentiation of basal cell carcinoma of Ptch mutant mice via CaMKII. Cancer Research 70: 2739-48
- Uhmann A, Dittmann K, Nitzki F, Dressel R, Koleva M, Frommhold A, Zibat A, Binder C, Adham I, Nitsche M, Heller T, Armstrong V, Schulz-Schaeffer W, Wienands J, Hahn H (2007) The Hedgehog receptor Patched controls lymphoid lineage commitment. Blood 110: 1814-23
- Hahn H, Wicking C, Zaphiropoulos P, Gailani M, Shanley S, Chidambaram A, Vorechovsky I, Holmberg E, Unden A, Gillies S, Negus K, Smyth I, Pressman C, Leffell D, Gerrard B, Goldstein A, Wainright B, Toftgard R, Chenevix-Trench G, Dean M, Bale A (1996) Mutations of the human homologue of Drosophila patched in the nevoid basal cell carcinoma syndrome. Cell 85: 841-51