Liz Wayne

  PhD Student

 Principal Investigator:
         Dr. Schaffer

The 5-year survival rate for breast cancer that is treated while the tumor is still localized is 98%. However, the survival rate for breast cancer that has metastasized plummets to 23%.1 This devastating trend is replicated for all types of cancer. Metastasis is the leading cause of death in cancer patients because of the difficulty to treat the secondary tumors and the latency period between dissemination of metastatic cells from the primary tumor to other sites and clinical detection. As such, metastasis accounts for a considerable bulk of the $100 billion yearly cost of cancer medical treatment. Understanding the mechanisms underlying metastasis events could have an enormous impact on patient survival rates and how clinicians and scientists target drugs to reduce metastasis. Current research focuses on receptors pathways, suggesting that the microenvironment of the secondary host creates a “metastatic niche” that explains why certain cancers consistently spread to specific organs. There is reason, however, to believe that hemodynamic forces are also essential in metastasis, although they have received less attention. Previous studies measured the migration velocity and deformation of circulating tumor cells (CTCs) in vessels, but most have been done in non -mammalian models and few have definitely shown the extent to which hemodynamic forces and vessel shape determine where CTCs arrest in vasculature. Micro-stroke data from my lab indicate that a vessel occlusion induces a severe decrease in blood flow downstream of the event, leading to ischemia. Other work shows that such ischemia leads to up-regulation of adhesion molecules such as ICAM and e-selectin.6 ICAM and e-selectin are also known to interact with tumor cells in circulation, and may provide a molecular mediator of CTC extravasation through vessels. I propose that tumor cells initial occlusion of vessels by mechanical plugging leads to ischemia that induces inflammatory responses and aids extravasation. My research will integrate novel information known about CTC/endothelial cell interactions with mechanical, hemodynamic mechanisms, and use two photon-microscopy in live animals to gain a more holistic view of extravasation during metastasis. I will characterize adhesion and extravasation dynamics of ischemic areas in microvasculature. Also I will look at the role of ischemia in adhesion molecule up regulation. I received my bachelors’ degree in Physics from the University of Pennsylvania in 2009. Currently, I am working towards a PhD in Biomedical Engineering at Cornell. I am very active in outreach and the broader scientific community. At Cornell, I am the BMES Newsletter Editor. We produce one newsletter a month. I am also involved in organizing outreach activities such as gathering IHC slides to donate to science classrooms. I am a member of the National Society of Black Physicists and the Biomedical Engineering Society. For fun, I enjoy cooking, watching comedy shows, black and white photography, and good science fiction books. I am an HHMI Med-Into-Grad fellow.

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