1. Development of novel cancer therapies

We are particularly interested in developing novel treatment options for rare forms of cancer, as well as for cancers that do not respond to current forms of therapy. One example is mast cell leukemia, a rare but extremely aggressive form of leukemia with little treatment options and dismal prognosis. Another example is drug-resistant chronic myeloid leukemia (CML), which can also be difficult to treat. Using methods originally developed for yeast research, we have designed a powerful cell competition assay that we are using for high-throughput screening of large drug libraries. The goal of these screens is to identify compounds that specifically kill oncogene-expressing cells while leaving isogenic, untransformed cells unharmed. This project is sponsored by a persoanlized medicine grant from the Norwegian Cancer Society.

2. Personalized medicine for AML and CML patients

Acute myeloid leukemia (AML) is a common form of cancer. Unfortunately, AML has a relatively poor survival rate, especially for elderly patients who often do not tolerate the aggressive chemotherapy that is used to treat this disease. Further complicating effective treatment of patients is the fact that AML can be caused by a heterogeneous set of mutations, and it is believed that this heterogeneic nature of the disease is one of the underlying causes for chemotherapy failure. Sponsored by the personalized medicine grant from the Norwegian Cancer Society already mentioned above, we are collaborating with clinicians at Oslo University Hospital to develop a method for individualized treatment of AML patients. The ultimate goal is to provide treatment for patients that currently do not qualify for standard of care treatment, and for patients that have failed chemotherapy.

3. Oncogene addiction

Our cancer research projects are primarily focused on oncogene addiction. Oncogene addiction is the puzzling phenomenon in which cells which have been exposed to the activity of a specific oncogene for a certain period of time suddenly become critically dependent upon the continuous activity of that oncogene for their survival. In this process, the oncogene somehow re-wires cellular survival pathways. How this is accomplished is not well understood, although it has been suggested to involve irreversible alterations of transcriptional programs. We are particularly interested in unraveling the mechanisms by which these oncogenes re-wire the transcriptional circuitries of cells.