Author

M. J. Arends

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 Pharmacology & Toxicology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 3 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell type annotation· 2 Research Focus:host-pathogen & immune response· 2 Research Focus:development & morphogenesis· 1 Research Focus:differential expression· 1 Assay:DNA methylation· 1

Frequent Co-Authors

A. Lima· 1 shared A. Valanciute· 1 shared A.-M. Ochocka-Fox· 1 shared D. Laurent· 1 shared E. Rose· 1 shared F. Semple· 1 shared F. V. N. Din· 1 shared G. I. Evan· 1 shared

Activity by Year

2019-2019 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 16 mutual co-author links

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Curved chords = mutual co-authorship

1 shared paperCancer Biology

A. Lima

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Aspirin-mediated DKK-1 increase rescues Wnt-driven stem-like phenotype in human intestinal organoids

K. Dunbar, A. Valanciute, V. Rajasekaran, T. Jamieson, P. Freile Vinuela, A. Lima, J. Blackmur, A.-M. Ochocka-Fox, M. J. Arends, O. J. Sansom, K. B. Myant, S. M. Farrington, M. G. Dunlop, F. V. N. Din

The paper shows aspirin reduces Wnt-driven stem-like traits in intestinal organoids by increasing DKK-1, suggesting a mechanism for its anti-cancer effects.

bioRxiv · Oct 17, 2019 · PreprintCancer Biology

Absolute measurement of the tissue origins of cell-free DNA in the healthy state and following paracetamol overdose

D. Laurent, F. Semple, P. J. Starkey Lewis, E. Rose, H. A. Black, S. J. Forbes, M. J. Arends, J. W. Dear, T. J. Aitman

This study directly measures the tissue origins of cell-free DNA in healthy mice and after paracetamol overdose, showing increased liver contribution in cases of liver injury.

bioRxiv · Jul 26, 2019Pharmacology & Toxicology

Myc instructs and maintains pancreatic adenocarcinoma phenotype

N. M. Sodir, R. M. Kortlever, V. J. Barthet, L. Pellegrinet, T. Campos, S. Kupczak, L. Brown Swigart, L. Soucek, M. J. Arends, T. D. Littlewood, G. I. Evan

This study shows Myc activation in PanIN cells drives the transition to PDAC by instructing a fibroinflammatory stroma, and its deactivation reverses the phenotype, suggesting Myc as a reversible molecular switch for PDAC.

bioRxiv · Feb 21, 2019Cancer Biology