Bio

Honors & Awards


  • Stanford Graduate Fellowship, Vice Provost for Graduate Education, Stanford University (2018-2021)
  • Leave Term Grant (Kaminsky Academic Enrichment Award), Dartmouth College (2017)
  • William H. Neukom 1964 Scholar, Neukom Institute, Dartmouth College (2017)
  • James O. Freedman Presidential Scholar, Dartmouth College (2016)
  • Sophomore Science Scholar (Bingham Undergraduate Research Award), Dartmouth College (2016)

Professional Affiliations and Activities


  • Associate Member, Sigma Xi (2018 - Present)
  • Student Member, American Association for Cancer Research (2018 - Present)
  • Student Member, Society for Neuro-Oncology (2018 - Present)

Education & Certifications


  • B.A., Dartmouth College, Biology (High Honors) (2018)

Publications

All Publications


  • Secretion-mediated STAT3 activation promotes self-renewal of glioma stem-like cells during hypoxia ONCOGENE Bonnin, D., Havrda, M. C., Lee, M. C., Liu, H., Zhang, Z., Nguyen, L. N., Harrington, L. X., Hassanpour, S., Cheng, C., Israel, M. A. 2018; 37 (8): 1107–18

    Abstract

    High-grade gliomas (HGGs) include the most common and the most aggressive primary brain tumor of adults and children. Despite multimodality treatment, most high-grade gliomas eventually recur and are ultimately incurable. Several studies suggest that the initiation, progression, and recurrence of gliomas are driven, at least partly, by cancer stem-like cells. A defining characteristic of these cancer stem-like cells is their capacity to self-renew. We have identified a hypoxia-induced pathway that utilizes the Hypoxia Inducible Factor 1α (HIF-1α) transcription factor and the JAK1/2-STAT3 (Janus Kinase 1/2 - Signal Transducer and Activator of Transcription 3) axis to enhance the self-renewal of glioma stem-like cells. Hypoxia is a commonly found pathologic feature of HGGs. Under hypoxic conditions, HIF-1α levels are greatly increased in glioma stem-like cells. Increased HIF-1α activates the JAK1/2-STAT3 axis and enhances tumor stem-like cell self-renewal. Our data further demonstrate the importance of Vascular Endothelial Growth Factor (VEGF) secretion for this pathway of hypoxia-mediated self-renewal. Brefeldin A and EHT-1864, agents that significantly inhibit VEGF secretion, decreased stem cell self-renewal, inhibited tumor growth, and increased the survival of mice allografted with S100β-v-erbB/p53-/- glioma stem-like cells. These agents also inhibit the expression of a hypoxia gene expression signature that is associated with decreased survival of HGG patients. These findings suggest that targeting the secretion of extracellular, autocrine/paracrine mediators of glioma stem-like cell self-renewal could potentially contribute to the treatment of HGGs.

    View details for DOI 10.1038/onc.2017.404

    View details for Web of Science ID 000425905700013

    View details for PubMedID 29155422

    View details for PubMedCentralID PMC5851110