Author

D. W. Scott

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

Frequent Co-Authors

C. Steidl· 3 shared A. Telenius· 2 shared K. Takata· 2 shared P. Farinha· 2 shared A. Chadburn· 1 shared A. Gamboa· 1 shared A. Jiang· 1 shared A. Karsan· 1 shared

Activity by Year

2021-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 35 mutual co-author links

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3 shared papersCancer Biology

C. Steidl

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3 papers

Recent·Most cited

The spatially resolved tumor microenvironment predicts treatment outcome in relapsed/refractory Hodgkin lymphoma

T. Aoki, A. Jiang, A. Xu, Y. Yin, A. Gamboa, K. Milne, K. Takata, T. Miyata-Takata, S. Wu, M. Warren, C. Strong, T. Goodyear, K. Morris, L. C. Chong, M. Hav, , C. Steidl

The paper develops a prognostic model using spatially resolved tumor microenvironment features to predict treatment outcomes in relapsed/refractory Hodgkin lymphoma.

bioRxiv · May 19, 2023Cancer Biology

Cooperative super-enhancer inactivation caused by heterozygous loss of CREBBP and KMT2D skews B cell fate decisions and yields T cell-depleted lymphomas

J. Li, C. R. Chin, H.-Y. Ying, C. Meydan, M. R. Teater, M. Xia, P. Farinha, K. Takata, C.-S. Chu, M. A. Rivas, A. Chadburn, C. Steidl, D. W. Scott, R. G. Roeder, C. E. Mason, , A. M. Melnick

This study shows that combined loss of CREBBP and KMT2D disrupts super-enhancer function in B cells, leading to immune evasion and T cell depletion in lymphomas.

bioRxiv · Feb 13, 2023Cancer Biology

Non-coding NFKBIZ 3' UTR mutations promote cell growth and resistance to targeted therapies in diffuse large B-cell lymphoma

S. E. Arthur, J. Gao, S. Healy, C. K. Rushton, N. Thomas, L. K. Hilton, K. Dreval, J. Tang, M. Alcaide, R. Cojocaru, A. Mottok, A. Telenius, P. Unrau, W. H. Wilson, L. M. Staudt, , R. D. Morin

This study identifies non-coding NFKBIZ 3' UTR mutations as drivers of DLBCL growth and resistance to NF-κB-targeted therapies, suggesting their potential as biomarkers.

bioRxiv · May 22, 2021 · PreprintCancer Biology