Author

M. Copland

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· 2 Cell Biology· 2

Signature Assays, Organisms & Methods

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Organism:human· 4 Assay:bulk RNA-seq· 3 Research Focus:differential expression· 3 Research Focus:cancer & tumor microenvironment· 2 Research Focus:drug response / drug discovery· 2 Approach:experimental assay· 2 Approach:statistical model· 2 Research Focus:cell type annotation· 1

Frequent Co-Authors

K. Kirschner· 2 shared T. Holyoake· 2 shared A. C. Purcell· 1 shared A. Dawson· 1 shared A. E. Davis· 1 shared A. Fawkes· 1 shared A. Ianniciello· 1 shared A. Newcombe· 1 shared

Activity by Year

2020-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 16 mutual co-author links

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2 shared papersCell Biology

K. Kirschner

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Author profile →

4 papers

Recent·Most cited

Mitochondrial folate metabolism inhibition drives differentiation through mTORC1 mediated purine sensing

M. M. Zarou, K. M. Rattigan, D. Sarnello, A. Dawson, A. Ianniciello, K. Dunn, M. Copland, D. Sumpton, A. Vazquez, V. Helgason

The paper shows that inhibiting mitochondrial folate metabolism drives differentiation in CML cells via mTORC1 and purine sensing, and enhances the efficacy of imatinib in reducing therapy-resistant LSCs.

bioRxiv · Dec 21, 2022 · PreprintCancer Biology

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

Longitudinal dynamics of clonal hematopoiesis identifies gene-specific fitness effects

N. A. Robertson, E. Latorre-Crespo, M. Terrada-Terradas, A. C. Purcell, B. J. Livesey, J. A. Marsh, L. Murphy, A. Fawkes, L. MacGillvray, M. Copland, R. E. Marioni, S. E. Harris, S. R. Cox, I. J. Deary, L. J. Schumacher, , T. Chandra

This study quantifies gene-specific fitness effects of CHIP drivers over 12 years using longitudinal sequencing data and a new DIF filtering method, showing gene-specific differences can inform personalized clinical management.

bioRxiv · May 27, 2021Cell 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