Human polyomaviruses

Human polyomaviruses (HPyVs) are small dsDNA viruses that infect most people. So far, 12 human polyomaviruses have been identified and antibodies against each of them can be detected in >50% of the subjects examined. HPyVs seem to establish a harmless life-long infection in healthy subjects. However, in immunocompromised patients, HPyVs can reactivate and may cause kidney defects, progressive multifocal leukoencephalopathy or trichodysplasia spinulosa. One HPyV, Merkel cell polyomavirus, is associated with Merkel cell carcinoma, a rare, but aggressive skin cancer. Little is known about the natural host cells of these viruses. We study the transcriptional activity of these viruses in different cell types and investigate signalling pathways that may lead to reactivation.

Neuroblastom

Målsetningen med dette prosjektet er å finne frem nye behandlingsformer for  neuroblastom, nervecelletumorer hos barn. Vi har tidligere vist at inflammatoriske mediatorer, fremfor alt eikosanoider, er viktige for at tumoren skal kunne vokse, invadere andre vev og spre seg. Ved å studere og forstå mekanismene bak syntesen av eikosanoider og andre inflammatoriske mediatorer og spesielt hvordan disse bidrar til cytostatika resistens og immunsuppressjon har man et håp om å kunne utvikle nye droger som kan hemme denne syntesen effektivt og dermed minske tumorvekst. Potensialet ligger fremfor alt i å anvende slike droger som tilleggsbehandling til sammen med konvensjonell behandling med cytostatika med mål å kunne  potensiere cytostatikans effekt og samtidig minske seneffekter som kan oppstå hos barn behandlet for kreft. Vår forskning går ut på å undersøke og forstå betydningen av inflammatoriske celler og mediatorer i nervecelltumører hos barn med håp om å kunne senere tilby bedre behandling.

Signal transduction pathways

Research in our group focuses on the mitogen-activated protein kinase (MAPK) pathway and the cAMP/cAMP-dependent protein kinase (cAMP/PKA) pathway. Both pathways paly import roles in cellular processes such as proliferation, differentiation, cell survival, cell death, migration, and gene regulation. Extensive interaction (cross-talk) exists between the MAPK and PKA pathways. We are especially interested in MK5/PRAK, a protein kinase that belongs to the MAPK pathway. MK5/PRAK has been shown to possess tumorigenic, as well as tumour suppressive properties in cell culture and in animal models. We elaborate on the molecular mechanisms of this protein in tumorigenesis and try to identify novel specific inhibitors against MK5/PRAK which can be used in cancer therapy.