Henrik Huitfeldt (Toxicopathology)
Group Leader: Henrik S. Huitfeldt Professor, M.D. , Ph.D.
Group Members:
Ellen Skarpen (PhD/post-doc)
Morten Oksvold (PhD/post-doc)
Lene Wierød (PhD student)
Carola Rosseland (PhD student)
Helga Grøsvik (Bioengineer)
Liv Ingrid Flinder (Medical student)
Svanhild Zirin Slåtto (Medical student)
Our group aims at clarifying the initial steps of carcinogenesis; how some cells escape the mitoinhibitory effects of environmental carcinogens to become initiated cells, and thereafter expand to preneoplastic lesions. To study alterations in growth factor signalling and cell cycle regulation. We use an experimental rat liver carcinogenesis model, and have developed corresponding primary hepatocyte culture models, To reflect environmental carcinogens, the DNA-damaging polyaromatic hydrocarbon 2-acetylaminofluorene, is employed. In addition, prototype non-DNA damaging carcinogens (dioxin-like and non-dioxin-like polychlorinated biphenyls), are studied. In particular, EGF receptor activation of PI3K and MAPK pathways, and how these regulate Cdk2, Cdk4 and p53 during carcinogen exposure, are studied. We also maintain a core facility for advanced light microscopy for the Gaustad campus. We offer training and provide access to confocal microscopy and image analysis. The Laboratory participates in Center for Cellular Stress Responses, one of the Thematic Research Areas at the Faculty of Medicine.
Latest publications:
Activation of the p53-p21(Cip1) pathway is required for CDK2 activation and S-phase entry in primary rat hepatocytes
Oncogene. 2007 Nov 19; [Epub ahead of print]
Wierød L, Rosseland CM, Lindeman B, Oksvold MP, Grøsvik H, Skarpen E, Huitfeldt HS.
CDK2 regulation through PI3K and CDK4 is necessary for cell cycle progression of primary rat hepatocytes.
Cell Prolif. 2007 Aug;40(4):475-87
MEK1 and MEK2 regulate distinct functions by sorting ERK2 to different intracellular compartments.
