Author

M. Vanneste

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 Bioengineering· 1

Signature Assays, Organisms & Methods

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Research Focus:cancer & tumor microenvironment· 2 Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:cell type annotation· 1 Research Focus:clustering· 1 Approach:contrastive learning· 1 Approach:deep learning· 1 Organism:human· 1

Frequent Co-Authors

P. Breheny· 2 shared A. C. Rowat· 1 shared B. D. Hallgrimsson· 1 shared B. L. Krog· 1 shared C. S. Stipp· 1 shared C. Yong· 1 shared D. L. Moose· 1 shared D. Moose· 1 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 16 mutual co-author links

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2 shared papersCancer Biology

P. Breheny

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

A 3D Clinical Face Phenotype Space of Genetic Syndromes using a Triplet-Based Singular Geometric Autoencoder

S. S. Mahdi, E. Caldeira, H. Matthews, M. Vanneste, N. Nauwelaers, M. Yuan, S. Gong, G. Bouritsas, G. S. Baynam, P. Hammond, R. Spritz, O. D. Klein, M. Bronstein, B. D. Hallgrimsson, H. Peeters, P. Claes

This paper develops a triplet-based geometric autoencoder to create a clinical face phenotypic space for syndrome diagnosis, showing it can classify syndromes, generalize to new ones, and preserve genetic disease relationships.

bioRxiv · Dec 27, 2022Bioengineering

Locally-invasive, castrate-resistant prostate cancer in a Pten/Trp53 double knockout mouse model of prostate cancer monitored with non-invasive bioluminescent imaging

C. Yong, D. Moose, N. Bannick, M. Vanneste, R. Svensson, P. Breheny, J. Brown, M. Cohen, M. Henry

The paper improves a prostate cancer mouse model with a bioluminescent reporter to monitor tumor progression and shows that double knockout of Pten and Trp53 leads to castrate-resistant, locally invasive tumors.

bioRxiv · Apr 23, 2020Cancer Biology

Cancer cells resist mechanical destruction in the circulation via RhoA-myosin II axis

D. L. Moose, B. L. Krog, L. Zhao, T.-H. Kim, S. Williams-Perez, G. Burke, L. Rhodes, M. Vanneste, P. Breheny, M. Milhem, C. S. Stipp, A. C. Rowat, M. D. Henry

This study identifies the RhoA-myosin II axis as a mechanism enabling cancer cells to resist mechanical destruction by hemodynamic forces in circulation.

bioRxiv · Apr 6, 2019Cancer Biology