The health of an organism is linked to the tightly regulated balance between cell proliferation and cell death. Any aberrant tilt in this balance can lead to devastating human diseases. For example, excessive proliferation unbalanced by cell death leads to cancer. On the opposite end of the spectrum, excessive cell death unbalanced by proliferation causes degenerative diseases such as Alzheimer’s, Parkinson’s and Amyotrophic Lateral Sclerosis. In the Andersen lab, we use a combination of molecular and proteomics approaches to understand the mechanisms that govern this balance and how they go awry in disease. A better understanding of these processes gives us the tools to develop more targeted and effective therapies.
The mechanisms by which cancer cells develop resistance to therapy— Chemotherapy is the primary mode of treatment for the majority of cancers and is often the only viable treatment option. Although the initial tumor response to chemotherapy is generally positive, many tumors possess a dynamic ability to adapt and develop resistance to chemotherapy (termed “chemoresistance”), which is the most common cause of patient mortality. A major roadblock to solving this problem is our fragmented understanding of the mechanisms that cause chemoresistance in tumors. To address this problem, a central project in our lab focuses on the protein 14-3-3z, a cellular hub that orchestrates many chemoresistance-promoting mechanisms. Our ongoing work in this area has uncovered a variety molecular switches that control fundamental cancer processes, such as cell cycle progression, autophagy and pro-survival kinase signaling. Based on these projects, we have identified cancer vulnerabilities that we are currently working to exploit in order to improve cancer therapeutics.