Bio

Brandon Hwa-Lin Bergsneider, from Los Angeles, CA, is pursuing an MD at Stanford School of Medicine. Brandon earned a bachelor of science in human biology from Stanford, and a MSc in bioinformatics and theoretical systems biology from Imperial College London. Brandon aspires to use data science-based technologies to advance health equity through early diagnosis, democratizing health information, and improving treatment efficacy. At Stanford and Imperial, he researched the molecular bases of neurodegeneration, the genetic susceptibility of neuroblastoma patients to SARS-CoV-2, computational protein structure prediction, and using machine learning to identify chemotherapy-resistant cancer cells. Brandon has also worked at the National Institutes of Health, where he used computational network analysis to identify clinical and demographic determinants of brain tumor patient symptom burden. Brandon has multiple first-author publications and, outside of academics, enjoys volunteering as a surf-therapy instructor for military veterans. He is a Knight-Hennessy Scholar, a Fulbright Scholar, and an NIH Cancer Research Training Award Fellow.

Contact

  • Academic
    bbergs@stanford.edu
    University - Student Department: School of Medicine Position: Graduate, Medicine

All Publications

  • CCR2 and CCR5 co-inhibition modulates immunosuppressive myeloid milieu in glioma and synergizes with anti-PD-1 therapy. Oncoimmunology Pant, A., Hwa-Lin Bergsneider, B., Srivastava, S., Kim, T., Jain, A., Bom, S., Shah, P., Kannapadi, N., Patel, K., Choi, J., Cho, K. B., Verma, R., Yu-Ju Wu, C., Brem, H., Tyler, B., Pardoll, D. M., Jackson, C., Lim, M. 2024; 13 (1): 2338965

    Abstract

    Immunotherapy has revolutionized the treatment of cancers. Reinvigorating lymphocytes with checkpoint blockade has become a cornerstone of immunotherapy for multiple tumor types, but the treatment of glioblastoma has not yet shown clinical efficacy. A major hurdle to treat GBM with checkpoint blockade is the high degree of myeloid-mediated immunosuppression in brain tumors that limits CD8 T-cell activity. A potential strategy to improve anti-tumor efficacy against glioma is to use myeloid-modulating agents to target immunosuppressive cells, such as myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment. We found that the co-inhibition of the chemokine receptors CCR2 and CCR5 in murine model of glioma improves the survival and synergizes robustly with anti-PD-1 therapy. Moreover, the treatment specifically reduced the infiltration of monocytic-MDSCs (M-MDSCs) into brain tumors and increased lymphocyte abundance and cytokine secretion by tumor-infiltrating CD8 T cells. The depletion of T-cell subsets and myeloid cells abrogated the effects of CCR2 and CCR5 blockade, indicating that while broad depletion of myeloid cells does not improve survival, specific reduction in the infiltration of immunosuppressive myeloid cells, such as M-MDSCs, can boost the anti-tumor immune response of lymphocytes. Our study highlights the potential of CCR2/CCR5 co-inhibition in reducing myeloid-mediated immunosuppression in GBM patients.

    View details for DOI 10.1080/2162402X.2024.2338965

    View details for PubMedID 38590799

    View details for PubMedCentralID PMC11000615

  • Next-Generation Sequencing and Personalized Medicine for Brain Cancer CURRENT SURGERY REPORTS Bergsneider, B. H., Liau, L. M. 2018; 6 (12)

    View details for DOI 10.1007/s40137-018-0221-x

    View details for Web of Science ID 000447654500002