Author

M. de Wit

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· 2 Organism:human· 2 Assay:proteomics· 2 Research Focus:cancer & tumor microenvironment· 1 Assay:DNA methylation· 1 Research Focus:drug response / drug discovery· 1 Research Focus:host-pathogen & immune response· 1 Organism:mouse· 1

Frequent Co-Authors

I. de Heer· 2 shared A. Brandes· 1 shared A. Gijtenbeek· 1 shared A. Kok· 1 shared A. Nowak· 1 shared A. Z. Mykytyn· 1 shared B. Baumert· 1 shared B. Haagmans· 1 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 20 mutual co-author links

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2 shared papersCancer Biology

I. de Heer

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Omicron BA.1 and BA.2 are antigenically distinct SARS-CoV-2 variants

A. Z. Mykytyn, M. Rissmann, A. Kok, M. Rosu, D. Schipper, T. I. Breugem, P. B. van den Doel, F. Chandler, T. Bestebroer, M. de Wit, M. E. van Royen, R. Molenkamp, B. Oude Munnink, R. D. de Vries, C. GeurtsvanKessel, , B. Haagmans

This study compares the antigenic differences between SARS-CoV-2 Omicron BA.1 and BA.2 variants using antigenic cartography and hamster sera, finding they are distinct antigenic outliers.

bioRxiv · Feb 23, 2022 · PreprintMicrobiology

DNA methylation and survival differences associated with the type of IDH mutation in 1p/19q non-codeleted astrocytomas

M. Tesileanu, W. Vallentgoed, M. Sanson, W. Taal, P. Clement, W. Wick, A. Brandes, J.-F. Baurain, O. Chinot, H. Wheeler, S. Gill, M. Griffin, L. Rogers, R. Ruda, M. Weller, , van den Bent

The paper shows that IDH mutations other than p.R132H in 1p/19q non-codeleted astrocytomas are linked to higher DNA methylation and better patient survival.

bioRxiv · Dec 10, 2020 · PreprintCancer Biology

Effective Tyrosine Kinase Inhibitors result in the intracellular accumulation of EGFR and allows response prediction in patients

M. de Wit, Y. Gao, D. Mercieca, I. de Heer, B. Valkenburg, M. van Royen, J. Aerts, P. Sillevis Smitt, P. French

The paper shows that EGFR tyrosine kinase inhibitors (TKIs) cause intracellular EGFR accumulation only in specific mutation-TKI combinations, which predicts clinical response in patients.

bioRxiv · Oct 21, 2019 · PreprintCancer Biology