Author

T. Holyoake

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· 1 Cell Biology· 1

Signature Assays, Organisms & Methods

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Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Approach:experimental assay· 1 Organism:mouse· 1 Approach:statistical model· 1

Frequent Co-Authors

M. Copland· 2 shared A. E. Davis· 1 shared A. Newcombe· 1 shared A.-L. Latif· 1 shared B. Higgens· 1 shared C. McKeeve· 1 shared C. Munje· 1 shared C. Reid· 1 shared

Activity by Year

2020-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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2 shared papersCancer Biology

M. Copland

Mutual co-authors in cluster

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2 papers

Recent·Most cited

Tyrosine kinase inhibitor independent gene expression signature in CML offers new targets for LSPC eradication therapy

E. Gomez-Castaneda, S. Rogers, C. Munje, J. Bittencourt-Silvestre, M. Copland, D. Vetrie, L. Hopcroft, H. Jorgensen, T. Holyoake

The paper identifies TKI-independent genes in CML LSC that could be targeted for new therapies, showing that gemtuzumab-ozogamicin and cyclosporine A have stronger effects on CML cells than healthy cells.

Cancers · Oct 26, 2022Peer-reviewedCancer Biology

BRD4-mediated repression of p53 is a target for combination therapy in AML

A.-L. Latif, A. Newcombe, S. Li, K. Gilroy, N. Robertson, X. Lei, H. Stewart, J. Cole, M. T. Terradas, L. Rishi, L. McGarry, C. McKeeve, C. Reid, W. Clark, J. Campos, , P. D. Adams

This study shows that combining MDM2 inhibitors and BET inhibitors synergistically kills AML cells by enhancing p53 activation through BRD4's repressive function.

bioRxiv · Sep 16, 2020Cell Biology