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
My research encompasses reproductive physiology and includes projects that involve both ovarian cancer as well as preterm birth. Preterm birth (birth before 37 completed weeks of pregnancy) is the leading perinatal health complication globally, and is the leading cause of deaths in children younger than 5 years old. Fifteen million babies worldwide are born preterm annually; 1 million will die, and many of those who survive will have adverse future health outcomes. Currently, there are no effective means to diagnose and predict who is truly at risk for preterm birth, nor to determine who needs treatment and/or transport. Neutrophils have been shown to play an important role in the process of both term and preterm labor by migrating from the peripheral blood to the uterus. Our lab analyzes neutrophils isolated from women in different stages of pregnancy to determine if there are surface, RNA, or protein content changes in the cells that can be detected in order to enhance our ability to predict preterm birth.
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. Cancer cells 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. 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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