Author

M. J. Fuchter

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 Microbiology· 1

Signature Assays, Organisms & Methods

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

Frequent Co-Authors

D. J. Murphy· 2 shared N. Brady· 2 shared S. Laing· 2 shared A. Barnard· 1 shared A. Lima· 1 shared A. Rueda-Zubiaurre· 1 shared B. Kruspig· 1 shared C. Miller· 1 shared

Activity by Year

2021-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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2 shared papersCancer Biology

D. J. Murphy

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

cMYC-mediated immune repression is reversed by inhibition of H3K9/H3K27 methylation maintenance

I. Dye, S. Laing, I. Garner, H. B. Mirza, N. Iyer, N. Brady, P. Spiliopoulou, S. Spear, J. Robinson, F. Fiorentino, M. J. Fuchter, D. J. Murphy, I. J. McNeish, R. Brown

This study shows that inhibiting H3K27/H3K9 methylation maintenance reverses cMYC-mediated immune repression in cancer, improving survival in mouse models.

bioRxiv · Oct 18, 2023 · PreprintCancer Biology

ERBB signalling contributes to immune evasion in KRAS-driven lung adenocarcinoma

S. Laing, B. Kruspig, R. Shaw, L. Officer-Jones, S. Edwards, D. McKinven, Y.-C. Hsieh, I. Powley, N. Brady, R. Pennie, R. Kwan, A. Lima, S. Myrta, M. Periyasamy, I. C. Dye, , D. J. Murphy

The paper investigates how ERBB signaling contributes to immune evasion in KRAS-driven lung adenocarcinoma using a novel mouse model and finds that transient ERBB blockade can restore immune surveillance when combined with PD1 blockade.

bioRxiv · Jul 24, 2023 · PreprintCancer Biology

Plasmodium falciparum protein Pfs16 is a target for transmission-blocking antimalarial drug development

S. Yahiya, C. N. Saunders, U. Straschil, O. J. Fischer, A. Rueda-Zubiaurre, S. Haase, G. Vizcay-Barrena, S. Jordan, S. Hassan, M. J. Delves, E. W. Tate, A. Barnard, M. J. Fuchter, J. Baum

This study identifies Pfs16 as the cellular target of the N-4HCS compound DDD01035881, which blocks Plasmodium male gamete formation.

bioRxiv · Jun 14, 2021Microbiology