Kelsey Hopland
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Kelsey Hopland has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Dana Wilkins
University of California, Berkeley–UCSF Graduate Program in Bioengineering, Berkeley, California, USA
1 shared publication - Erin A. Akins
University of California, Berkeley–UCSF Graduate Program in Bioengineering, Berkeley, California, USA
1 shared publication Kenny K.H. Yu
Department of Neurosurgery, Memorial Sloan Kettering Cancer Center, New York City, New York, USA
1 shared publication- Manish Kumar Aghi
Department of Neurological Surgery, University of California, San Francisco; and
1 shared publication - Robert C. Osorio
Department of Neurological Surgery, University of California, San Francisco, California, USA
1 shared publication - Sanjay Kumar
UC Berkeley Chemical and Biomolecular Engineering
1 shared publication
Latest Publications
- Open Access
- 22 August 2025
- Published by American Society for Clinical Investigation in JCI Insight
- Vol. 10 (16)
An engineered glioblastoma model yields macrophage-secreted drivers of invasion
While the accumulation of tumor-associated macrophages (TAMs) in glioblastoma (GBM) has been well documented, targeting TAMs has thus far yielded limited clinical success in slowing GBM progression due, in part, to an incomplete understanding of TAM function. Using an engineered 3D hydrogel–based model of the brain tumor microenvironment (TME), we show that M2-polarized macrophages stimulate transcriptional and phenotypic changes in GBM stem cells (GSCs) closely associated with the highly aggressive and invasive mesenchymal subtype. By combining proteomics with GBM patient single-cell transcriptomics, we identify multiple TAM-secreted proteins with putative proinvasive functions and validate TGF-β induced (TGFBI, also known as BIGH3) as a targetable TAM-secreted tumorigenic factor. Our work highlights the utility of coupling multiomics analyses with engineered TME models to investigate TAM–cancer cell crosstalk and offers insights into TAM function to guide TAM-targeting therapies.
- 22 August 2025
- Published by American Society for Clinical Investigation in JCI Insight
- Vol. 10 (16)
Open AccessAn engineered glioblastoma model yields macrophage-secreted drivers of invasion
While the accumulation of tumor-associated macrophages (TAMs) in glioblastoma (GBM) has been well documented, targeting TAMs has thus far yielded limited clinical success in slowing GBM progression due, in part, to an incomplete understanding of TAM function. Using an engineered 3D hydrogel–based model of the brain tumor microenvironment (TME), we show that M2-polarized macrophages stimulate transcriptional and phenotypic changes in GBM stem cells (GSCs) closely associated with the highly aggressive and invasive mesenchymal subtype. By combining proteomics with GBM patient single-cell transcriptomics, we identify multiple TAM-secreted proteins with putative proinvasive functions and validate TGF-β induced (TGFBI, also known as BIGH3) as a targetable TAM-secreted tumorigenic factor. Our work highlights the utility of coupling multiomics analyses with engineered TME models to investigate TAM–cancer cell crosstalk and offers insights into TAM function to guide TAM-targeting therapies.