Author

S. T. Keir

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cancer Biology· 3

Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 3 Approach:experimental assay· 3 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Organism:human· 2 Research Focus:host-pathogen & immune response· 1 Organism:mouse· 1

Frequent Co-Authors

D. M. Ashley· 3 shared Y. He· 3 shared C. J. Pirozzi· 2 shared H. Liu· 2 shared K. Roso· 2 shared M. S. Waitkus· 2 shared R. E. McLendon· 2 shared A. Briley· 1 shared

Activity by Year

2022-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

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3 shared papersCancer Biology

D. M. Ashley

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Author profile →

3 papers

Recent·Most cited

Interplay between ATRX and IDH1 mutations governs innate immune responses in diffuse gliomas

S. Hariharan, B. T. Whitfield, C. J. Pirozzi, M. S. Waitkus, M. C. Brown, M. L. Bowie, D. M. Irvin, K. Roso, R. Fuller, J. Hostettler, S. Dharmaiah, E. A. Gibson, A. Briley, A. Mangoli, C. Fraley, , D. M. Ashley

This study shows that ATRX loss primes glioma cells for innate immune recognition, while IDH1R132H mutation suppresses immune signaling, which can be reversed by IDH1 inhibition.

bioRxiv · Apr 20, 2023 · PreprintCancer Biology

Repurposing clemastine to target glioblastoma cell stemness

M. A. Sun, R. Yang, H. Liu, W. Wang, X. Song, B. Hu, N. Reynolds, K. Roso, L. H. Chen, P. K. Greer, S. T. Keir, R. E. McLendon, S.-Y. Cheng, D. D. Bigner, D. M. Ashley, , Y. He

This study shows clemastine, an antihistamine, reduces glioblastoma stemness by targeting EBP, a cholesterol pathway enzyme, and promotes differentiation of oligodendrocyte progenitor cells.

bioRxiv · Nov 5, 2022 · PreprintCancer Biology

Cancer-associated SMARCAL1 loss-of-function mutations promote alternative lengthening of telomeres and tumorigenesis in telomerase-negative glioblastoma cells

H. Liu, C. Xu, B. H. Diplas, A. Brown, L. M. Strickland, J. Ling, R. E. McLendon, S. T. Keir, D. M. Ashley, Y. He, M. S. Waitkus

This study shows SMARCAL1 loss-of-function mutations enable ALT in telomerase-negative glioblastoma cells, promoting tumorigenesis and telomere maintenance.

bioRxiv · Sep 19, 2022Cancer Biology