
Human haematopoietic stem cell lineage commitment is a continuous process (Nature Cell Biology, 2017)
Velten, L.*, Haas, S.F.*, Raffel, S.*, Blaszkiewicz, S., Islam, S., Hennig, B.P., Hirche, C., Lutz, C., Buss, E.C., Nowak, D., Boch, T., Hofmann, W.K., Ho, A.D., Huber, W., Trumpp, A.@, Essers, M.A.@, & Steinmetz, L.M.@ (2017). Human haematopoietic stem cell lineage commitment is a continuous process. Nature Cell Biology, 19(4), 271-281. doi: 10.1038/ncb3493 Cover Story *Shared first author @Shared corresponding author
Scientists at HI-STEM have uncovered a yet unknown mechanism for therapy resistance in pancreatic cancer based on overexpression of the enzyme CYP3A5. The paper was published in Nature Medicine.
Read more:
· DKFZ Press Release: Pancreatic Cancer: Enzyme renders tumors resistant
· Citation: Noll, E.M., Eisen, C., Stenzinger, A., Espinet, E., Muckenhuber, A., Klein, C., Vogel, V., Klaus, B., Nadler, W., Rosli, C., Lutz, C., Kulke, M., Engelhardt, J., Zickgraf, F.M., Espinosa, O., Schlesner, M., Jiang, X.Q., Kopp-Schneider, A., Neuhaus, P., Bahra, M., Sinn, B.V., Eils, R., Giese, N.A., Hackert, T., Strobel, O., Werner, J., Buchler, M.W., Weichert, W., Trumpp, A., & Sprick, M.R. (2016). CYP3A5 mediates basal and acquired therapy resistance in different subtypes of pancreatic ductal adenocarcinoma. Nature Medicine, 22(3), 278-287. doi: 10.1038/nm.4038
Dr. Michael Milsom was recently awarded the 2016 Fanconi Anemia Research Fund’s David B. Frohnmeyer Early Investigator Award. The award is given to independent investigators of high accomplishment within 10 years of starting their own group. Dr. Milsom is the second recipient of this award, which was established in 2015 in memory of David Frohnmayer, former Attorney General of the US state of Oregon, President of the University of Oregon, and founder of the Fanconi Anemia Research Foundation.
Dr. Milsom received this award in light of his pioneering work on the roles of DNA damage and Fanconi anemia signaling pathway function in governing the attrition of hematopoietic stem cells. Dr. Ray Monnat, Chair of the Fanconi Anemia Research Fund Scientific Advisory Board commented that “This is a topic of high, and growing, interest both within the Fanconi anemia community and experimental hematology in general.”
February 15, 2016
In a process called diapause, many animal species delay the development of their embryos in order to ensure that their offspring is born at a possibly favorable time. Scientists from DKFZ and HI-STEM have now shown that this process is regulated by the MYC oncogene. If MYC is turned off in mice, embryonic stem cells and early embryos enter a reversible biochemical state of dormancy. However, this does not affect their ability to differentiate into any cell type of the body. When MYC is reactivated, the dormant embryos are able to develop into healthy animals. These findings have been published in the latest issue of “Cell” and were featured as the cover story.
Read more:
· Citation: Scognamiglio, R., Cabezas-Wallscheid, N., Thier, M.C., Altamura, S., Reyes, A., Prendergast, A.M., Baumgartner, D., Carnevalli, L.S., Atzberger, A., Haas, S., von Paleske, L., Boroviak, T., Worsdorfer, P., Essers, M.A., Kloz, U., Eisenman, R.N., Edenhofer, F., Bertone, P., Huber, W., van der Hoeven, F., Smith, A., & Trumpp, A. (2016). Myc Depletion Induces a Pluripotent Dormant State Mimicking Diapause. Cell, 164(4), 668-680. doi: 10.1016/j.cell.2015.12.033