Author

M. S. Waitkus

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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Approach:experimental assay· 3 Assay:bulk RNA-seq· 2 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell type annotation· 2 Organism:human· 2 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:clustering· 1 Research Focus:differential expression· 1

Frequent Co-Authors

D. M. Ashley· 2 shared S. T. Keir· 2 shared Y. He· 2 shared A. Briley· 1 shared A. Brown· 1 shared A. J. Wisdom· 1 shared A. Mangoli· 1 shared B. H. Diplas· 1 shared

Activity by Year

2022-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 28 mutual co-author links

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2 shared papersCancer Biology

D. M. Ashley

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Author profile →

3 papers

Recent·Most cited

Loss of function of Atrx leads to activation of alternative lengthening of telomeres in a primary mouse model of sarcoma

M. Pierpoint, W. Floyd, A. J. Wisdom, L. Luo, Y. Ma, M. S. Waitkus, D. G. Kirsch

This study shows that loss of Atrx in a mouse sarcoma model activates the ALT telomere maintenance pathway independently of telomerase, leading to telomere instability and APB formation.

bioRxiv · Nov 6, 2023 · PreprintCancer Biology

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

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