In leukemia and in the development of carcinoma, several oncogenes / tumor suppressor genes cooperate to induce abnormal survival, proliferation, and developmental / behavioral plasticity in tumor cells, which may adopt properties of stem cells. Using both genetically modified mice and in vivo-like cell culture models, we focus on molecular mechanisms that transform hematopoietic stem cells into leukemia-initiating cells, and reprogram epithelial cells into primitive mesenchymal, stem cell-like cells during the progression of carcinoma and metastasis.
Lahsnig, C., Mikula, M., Petz, M., Zulehner, G., Schneller, D., van Zijl, F., Huber, H., Csiszar, A., Beug, H., Mikulits, W. (2009). ILEI requires oncogenic Ras for the epithelial to mesenchymal transition of hepatocytes and liver carcinoma progression.
Oncogene. 28(5):638-50
(abstract)
2006
Dolznig, H., Grebien, F., Deiner, EM., Stangl, K., Kolbus, A., Habermann, B., Kerenyi, MA., Kieslinger, M., Moriggl, R., Beug, H., Müllner, EW. (2006). Erythroid progenitor renewal versus differentiation: genetic evidence for cell autonomous, essential functions of EpoR, Stat5 and the GR.
Oncogene. 25(20):2890-900
(abstract)
Waerner, T., Alacakaptan, M., Tamir, I., Oberauer, R., Gal, A., Brabletz, T., Schreiber, M., Jechlinger, M., Beug, H. (2006). ILEI: a cytokine essential for EMT, tumor formation, and late events in metastasis in epithelial cells.
Cancer Cell. 10(3):227-39
(abstract)
