Jin Chen lab
HER2 is overexpressed in 15-20% of invasive breast cancers correlating to poor prognosis. HER2 is an orphan receptor tyrosine kinase (RTK) with no known ligand, and evidence suggests that HER2 overexpression leads to heterodimerization with ErbB2 recptor and cross-activation of other RTKs. Even though small molecule tyrosine kinase inhibitors and monoclonal antibodies such as Trastuzumab are initially effective in treating HER2-positive patients, long-term response rates are limited due to acquired resistance and relapse. The identification of new molecular targets is needed to improve long-term survival of HER2-positive patients. One goal of the Chen lab is looking at cancer metabolism and tumor immunity. The focus of my research is the identification of targets to inhibit cancer metabolism through signaling pathways that will eventually reverse tumor growth and immunosuppression.