Honors & Awards

  • Member of Omicron Theta Epsilon Biological Sciences Honor Society, CSU Chico (2004-2006)
  • Graduate Student Counsel Vice President, Univ. of Colorado Denver (2009-2010)
  • Predoctoral Research Fellow, Colorado Clinical and Translational Sciences Institute (CCTSI) (2009-2012)
  • Postdoctoral Research Fellow, Stanford Program in Epithelial Biology (2012-)

Professional Education

  • Doctor of Philosophy, University of Colorado Denver (2012)
  • Bachelor of Science, California State University, Chico (2006)

Stanford Advisors


Journal Articles

  • Growth differentiation factor-15 (GDF-15) suppresses in vitro angiogenesis through a novel interaction with connective tissue growth factor (CCN2) JOURNAL OF CELLULAR BIOCHEMISTRY Whitson, R. J., Lucia, M. S., Lambert, J. R. 2013; 114 (6): 1424-1433


    Growth differentiation factor-15 (GDF-15) and the CCN family member, connective tissue growth factor (CCN2), are associated with cardiac disease, inflammation, and cancer. The precise role and signaling mechanism for these factors in normal and diseased tissues remains elusive. Here we demonstrate an interaction between GDF-15 and CCN2 using yeast two-hybrid assays and have mapped the domain of interaction to the von Willebrand factor type C domain of CCN2. Biochemical pull down assays using secreted GDF-15 and His-tagged CCN2 produced in PC-3 prostate cancer cells confirmed a direct interaction between these proteins. To investigate the functional consequences of this interaction, in vitro angiogenesis assays were performed. We demonstrate that GDF-15 blocks CCN2-mediated tube formation in human umbilical vein endothelial (HUVEC) cells. To examine the molecular mechanism whereby GDF-15 inhibits CCN2-mediated angiogenesis, activation of αV β3 integrins and focal adhesion kinase (FAK) was examined. CCN2-mediated FAK activation was inhibited by GDF-15 and was accompanied by a decrease in αV β3 integrin clustering in HUVEC cells. These results demonstrate, for the first time, a novel signaling pathway for GDF-15 through interaction with the matricellular signaling molecule CCN2. Furthermore, antagonism of CCN2 mediated angiogenesis by GDF-15 may provide insight into the functional role of GDF-15 in disease states.

    View details for DOI 10.1002/jcb.24484

    View details for Web of Science ID 000317864800022

    View details for PubMedID 23280549

  • "Patch"ing Up Our Tumor Signaling Knowledge JOURNAL OF INVESTIGATIVE DERMATOLOGY Atwood, S. X., Whitson, R. J., Oro, A. E. 2013; 133 (5): 1131-1133


    The tumor suppressor Patched1 (Ptch1) possesses well-described roles in regulating sonic hedgehog (SHH) signaling in the skin and preventing the formation of basal cell carcinomas (BCCs). In this issue, Kang et al. extend their previous work to show that a naturally occurring allele of Ptch1 found in FVB mice promotes early squamous cell carcinoma (SCC) growth without aberrant activation of the SHH pathway. The study reveals new roles for Ptch1 that lie at the nexus between BCC and SCC formation.

    View details for DOI 10.1038/jid.2012.506

    View details for Web of Science ID 000317698800005

    View details for PubMedID 23594533

Stanford Medicine Resources: