Bio

Daniel Bernard Zamler is the son of Sherwin and Monica Zamler. After completing his work at Wylie E. Groves in Beverly Hills Michigan in 2009, he entered the University of Michigan in Ann Arbor, Michigan. He received the degree of Bachelor of Science with a major in Neuroscience from University of Michigan in May, 2013. For the next three years, he worked as a research technician in the Department of Neurosurgery at University of Michigan. In August of 2017 he entered The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences and completed in March of 2022.

Stanford Advisors

Contact

  • Academic
    dzamler@stanford.edu
    University - Scholar Department: Neurology Position: Postdoctoral Scholar

Additional Info

Research Interests

  • Achievement
  • Brain and Learning Sciences
  • Data Sciences
  • Higher Education
  • Math Education
  • Philosophy
  • Professional Development
  • Psychology
  • Research Methods
  • School Reform
  • Science Education
  • Secondary Education
  • Standards
  • Technology and Education

Current Research and Scholarly Interests

Working on the interface of Brain Tumors and Computer Science

All Publications

  • Intestinal toxicity to CTLA-4 blockade driven by IL-6 and myeloid infiltration. The Journal of experimental medicine Zhou, Y., Medik, Y. B., Patel, B., Zamler, D. B., Chen, S., Chapman, T., Schneider, S., Park, E. M., Babcock, R. L., Chrisikos, T. T., Kahn, L. M., Dyevoich, A. M., Pineda, J. E., Wong, M. C., Mishra, A. K., Cass, S. H., Cogdill, A. P., Johnson, D. H., Johnson, S. B., Wani, K., Ledesma, D. A., Hudgens, C. W., Wang, J., Wadud Khan, M. A., Peterson, C. B., Joon, A. Y., Peng, W., Li, H. S., Arora, R., Tang, X., Raso, M. G., Zhang, X., Foo, W. C., Tetzlaff, M. T., Diehl, G. E., Clise-Dwyer, K., Whitley, E. M., Gubin, M. M., Allison, J. P., Hwu, P., Ajami, N. J., Diab, A., Wargo, J. A., Watowich, S. S. 2023; 220 (2)

    Abstract

    Immune checkpoint blockade (ICB) has revolutionized cancer treatment, yet quality of life and continuation of therapy can be constrained by immune-related adverse events (irAEs). Limited understanding of irAE mechanisms hampers development of approaches to mitigate their damage. To address this, we examined whether mice gained sensitivity to anti-CTLA-4 (alphaCTLA-4)-mediated toxicity upon disruption of gut homeostatic immunity. We found alphaCTLA-4 drove increased inflammation and colonic tissue damage in mice with genetic predisposition to intestinal inflammation, acute gastrointestinal infection, transplantation with a dysbiotic fecal microbiome, or dextran sodium sulfate administration. We identified an immune signature of alphaCTLA-4-mediated irAEs, including colonic neutrophil accumulation and systemic interleukin-6 (IL-6) release. IL-6 blockade combined with antibiotic treatment reduced intestinal damage and improved alphaCTLA-4 therapeutic efficacy in inflammation-prone mice. Intestinal immune signatures were validated in biopsies from patients with ICB colitis. Our work provides new preclinical models of alphaCTLA-4 intestinal irAEs, mechanistic insights into irAE development, and potential approaches to enhance ICB efficacy while mitigating irAEs.

    View details for DOI 10.1084/jem.20221333

    View details for PubMedID 36367776

https://orcid.org/0000-0003-0375-8119