Education & Certifications


  • Master of Science, Stanford University, BIOE-MS (2018)
  • BS, Clemson University, Materials Science and Engineering (2016)

All Publications


  • Targeted glycan degradation potentiates the anticancer immune response in vivo. Nature chemical biology Gray, M. A., Stanczak, M. A., Mantuano, N. R., Xiao, H., Pijnenborg, J. F., Malaker, S. A., Miller, C. L., Weidenbacher, P. A., Tanzo, J. T., Ahn, G., Woods, E. C., Laubli, H., Bertozzi, C. R. 2020

    Abstract

    Currently approved immune checkpoint inhibitor therapies targeting the PD-1 and CTLA-4 receptor pathways are powerful treatment options for certain cancers; however, most patients across cancer types still fail to respond. Consequently, there is interest in discovering and blocking alternative pathways that mediate immune suppression. One such mechanism is an upregulation of sialoglycans in malignancy, which has been recently shown to inhibit immune cell activation through multiple mechanisms and therefore represents a targetable glycoimmune checkpoint. Since these glycans are not canonically druggable, we designed an alphaHER2 antibody-sialidase conjugate that potently and selectively strips diverse sialoglycans from breast cancer cells. In syngeneic breast cancer models, desialylation enhanced immune cell infiltration and activation and prolonged the survival of mice, an effect that was dependent on expression of the Siglec-E checkpoint receptor found on tumor-infiltrating myeloid cells. Thus, antibody-sialidase conjugates represent a promising modality for glycoimmune checkpoint therapy.

    View details for DOI 10.1038/s41589-020-0622-x

    View details for PubMedID 32807964