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Craig M Horbinski on Muck Rack

Craig M Horbinski

Jacksonville Beach
As seen in: Nature, Cell Press, The Journal of Clinical Investigation, Texas Medical Center, Chinese Clinical Oncology, Future Medicine, OncLive, Targeted Oncology, The Pathologist
Chair of the Department of Laboratory Medicine and Pathology at Mayo Clinic Florida. My #NIH-funded laboratory studies #glioma and #meningioma.
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Articles

Spatial chromatin architecture and accessibility co-profiling of mammalian tissues

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By Ping Wang, Juan Wang, Qixuan Wang, Mark W. Youngblood, Bo Tao, Josiah Wong, Yu Luan, Shaojun Yu, Alok Swaroop, Khizar R. Nandoliya, Hinda Najem, Yihao Fu, Kathleen McCortney, Di Zhang, Yarui Diao, Amy B. Heimberger, Adam M. Sonabend, Craig M Horbinski, Rong Fan, Feng Yue
| Nature Verified
Abstract Cellular function depends on the spatial organization of cells and biomolecules within the tissue microenvironment. Advances in spatial omics have enabled profiling of molecular features such as transcriptome, proteome and epigenome, and there has been rapid progress of imaging-based approaches to study spatial three-dimensional (3D) genome organization.
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Galanin impairs tumor immunity in glioblastoma by promoting infiltration and ferroptosis resistance of myeloid-derived suppressor cells

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By Lizhi Pang, Yang Liu Verified, Fei Zhou, Songlin Guo, Fatima Khan, Heba Ali, Hardik Shah, Sara Huber, Barbara Kofler, Craig M Horbinski, Peiwen Chen
| Nature Verified
Abstract Glioblastoma (GBM) is a highly aggressive and lethal form of brain tumor that resists immunotherapy. Here we show that neuropeptide galanin (GAL) drives immunosuppression and immunotherapy resistance in GBM. Mechanistically, GBM cell-secreted GAL interacts with its receptor GALR3 on monocytic myeloid-derived suppressor cells (mMDSCs), triggering USP51-mediated deubiquitination of estrogen receptor-α, thereby engaging membrane-bound O-acyltransferase domain-containing 1 signaling.
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Mismatch repair deficiency reshapes glioblastoma through immune suppression rather than hypermutation

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By Andrew Li, Thomas K. Sears, Craig M Horbinski
| The Journal of Clinical Investigation
Abstract Mismatch repair (MMR) deficiency is classically associated with microsatellite instability, a high tumor mutational burden (TMB), and sensitivity to immune checkpoint blockade in cancer. In this issue of the JCI, Puigdelloses Vallcorba et al. reported that this paradigm does not hold true in glioblastoma (GBM).
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