Author
M. van de Ven
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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2018-2022 · peak 3/yrCo-Author Collaboration Network
10 top collaborators · 26 mutual co-author links6 papers
Recent·Most cited
- Cancer BiologybioRxivDOI 10.1016/j.celrep.2023.112538
- Cancer BiologybioRxivPreprint
Combined SHP2 and ERK inhibition for the treatment of KRAS-driven Pancreatic Ductal Adenocarcinoma
K. J. Ciecielski, A. Mulero-Sanchez, A. Berninger…·S. Mainardi
This paper investigates the combination of SHP2 and ERK inhibition as a treatment for KRAS-driven pancreatic ductal adenocarcinoma, showing synergistic anticancer effects and tumor regression in mouse models.
DOI 10.1101/2021.12.14.472574 - Cancer BiologybioRxivPreprint
Loss of p16INK4a in neuroblastoma cells induces shift to an immature state with mesenchymal characteristics and increases sensitivity to EGFR inhibitors
N. A. Schubert, S. R. van Hooff, L. Schild…·M. L. van den Boogaard
DOI 10.1101/2021.10.27.465137 - Cancer BiologybioRxiv
Indisulam synergizes with palbociclib to induce senescence through inhibition of CDK2 kinase activity
Z. Pogacar, J. L. Johnson, L. Krenning…·R. Leite de Oliveira
The paper identifies that combining indisulam with palbociclib enhances senescence in cancer cells by inhibiting CDK2 kinase activity.
DOI 10.1371/journal.pone.0273182 - Cancer BiologybioRxivPreprint
Cancer modeling in colorectal organoids reveals intrinsic differences between oncogenic RAS and BRAF variants
J. B. Post, N. Hami, J. Lohuis…·H. J. G. Snippert
This study uses CRISPR to generate CRC organoids with different RAS pathway mutations, revealing distinct drug responses and growth patterns.
DOI 10.1101/860122 - Cancer BiologybioRxiv
Radiosensitivity is an acquired vulnerability of PARPi-resistant BRCA1-deficient tumors
M. Barazas, A. Gasparini, Y. Huang…·S. Rottenberg
This study identifies radiotherapy as a therapeutic target for BRCA1-deficient tumors that have developed resistance to PARP inhibitors through 53BP1 pathway inactivation.
DOI 10.1158/0008-5472.can-18-2077