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Jennifer Gubbels, Ph.D.



  • Assistant Professor, Physiology
  • Augustana University


  • Ph.D., Endocrinology-Reproductive Physiology, University of Wisconsin, Madison
  • B.S., Biological Research, Loras College, Dubuque, Iowa

Current Research: Ovarian Cancer (OvCa) is the seventh leading cause of cancer-related deaths in the United States and one of the most deadly gynecological diseases. The high level of mortality relates to the nature of OvCa progression, resulting in late-stage diagnosis and complicating treatment with current anti-cancer regimes. A relatively unexplored avenue of OvCa treatment is the hypercoagulative state of the OvCa tumor microenvironment. As such, it is necessary to better understand the role of the primary cellular component of coagulation, platelets, in cancer pathology in order to find more efficacious therapies that may limit the role of platelets. Platelet activation is normally a process that is initiated by damaged vascular tissue and catalyzes the coagulation cascade. Cancer cells also trigger platelet activation, resulting in platelet adherence to cancer cells and a subsequent release of platelet vesicle contents, including pro-mitotic, angiogenic, and metastatic factors. In addition, the adherent platelets can provide immune cloaking capability. Therefore, a rational choice for target selection would aim to disrupt the platelet-OvCa cell interaction. However, few cancer cell specific proteins that dictate cancer cell interactions with platelets have been identified. My lab, along with Dr. Mark Larson, aims to explore the role of the protein SUSD2 (Sushi Domain Containing 2), a novel cell surface protein enriched on the surface of OvCa cells that appears to prevent platelet/cancer cell interactions when compared to OvCa cells that lack SUSD2. We have also found that its expression correlates to dramatically improved patient survival times. Accordingly, it is one of the few proteins described to differentially affect cancer cell interactions with platelets, and is linked to a substantial clinical significance. In order to better understand this relationship, we will define the mechanism by which SUSD2 impairs platelet/OvCa cell interactions.

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