Cellular signal transduction and cancer pharmacology
The current understanding that oncogenes and tumor suppressor genes are mutated or dysregulated forms of normal genes encoding proteins involved in core pathways that control cellular processes such as proliferation, apoptosis, and motility, has led to enormous efforts to target these mechanisms pharmacologically in novel therapeutic strategies. However, due to the complexity of the mechanisms that are targeted, and the great tendency of cancer cells to develop resistance, further progress in the outcome of signal-directed therapies in cancer requires detailed insights into the tumor biology, signalling mechanisms, and pharmacology.
The research group focuses on basal cell biological and pharmacological studies of tumor-stroma interactions and cellular signalling mechanisms as possible targets for cancer treatment. The work is primarily directed at epithelial cancers of the gastrointestinal tract. It focuses on signalling involving a) receptor tyrosine kinases, in particular EGFR and Met, and b) G-protein-coupled receptors (GPCRs), particularly receptors for prostaglandins and lysophosphatidic acid.
- Mechanisms regulating signal transduction from EGFR and Met, with emphasis on the integration of their signalling pathways with those of GPCRs
- Mechanisms of non-genetic, adaptive, refractoriness to signal-directed antitumor therapy.
- Receptors and signalling mechanisms in tumor-stroma interactions.
Group leader Hege Thoresen, Department of Pharmacology, Tel: +47 22840213, E-mail: email@example.com