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B.A., University of Minnesota, Morris, MN 2014
Despite advances in therapies for breast cancer, this disease still remains a significant cause of mortality in women. Much interest surrounds the development of systemic novel targeted therapeutics, however, little is known about how these drugs affect the surrounding non-tumor cells within the tumor microenvironment. Understanding how systemically-delivered breast cancer-targeted therapies interact with non-tumor cells such as infiltrating macrophages is necessary for elucidating how cells become drug resistant and for developing more effective and durable therapies in cancer patients.
The Janus Kinase (JAK)/Signal Transducer and Activator of Transcription (STAT) signaling pathway is activated in breast cancer and when hyperactive, can influence uncontrollable proliferation and inflammation. New therapies aim to inhibit JAK/STAT signaling components to turn off the “switch” in tumors signaling for growth and proliferation. My research will involve looking at how inhibitors of the JAK/STAT pathway affect the tumor microenvironment. We hypothesize that although, inhibition of the JAK/STAT pathway may act on the primary tumor directly, the inhibitor alters a delicate balance in the microenvironment that pushes infiltrating macrophages from an anti-tumor immune response to a pro-inflammatory and thus, pro-tumorigenic response. I aim to delineate the signaling components responsible for creating this shift from tumor-hostile to tumor-friendly, as well as, developing combinatorial therapeutic strategies to target the tumor itself, as well as maintaining an anti-tumor response within the surrounding microenvironment.