Author

Tim H. Brümmendorf

RWTH Aachen UniversityORCID 0000-0002-9677-3723Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cancer Biology· 2

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1 Assay:scRNA-seq· 1

Frequent Co-Authors

Steffen KoschmiederiD· 2 shared Bärbel Junge· 1 shared Calvin Krollmann· 1 shared Carl Christian Kolbe· 1 shared Conny K. Baldauf· 1 shared Cristina Baquero López· 1 shared Dickson W.L. WongiD· 1 shared Dominik WolfiD· 1 shared

Activity by Year

2024-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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2 shared papersCancer Biology

Steffen KoschmiederORCID

Mutual co-authors in cluster

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2 papers

Recent·Most cited

Inhibition of JAK2V617F-Driven Neoplastic Endothelial Dysfunction by IFNα as a Novel Antifibrotic Mechanism

Madeline J. Caduc, Mohamed H. Elsafi Mabrouk, Martin Graßhoff, Pia Wanner, Katrin Götz, Jessica E. Pritchard, Dickson W.L. Wong, Cristina Baquero López, Louisa Böttcher, Pinar Sönmez, Bärbel Junge, Eva Miriam Buhl, Sabrina Ernst, Gerhard Müller‐Newen, Michael Vogt, , Marcelo A. S. Toledo

This study identifies JAK2V617F zygosity-specific vascular changes in MPN and shows IFNα inhibits EndMT, offering a novel antifibrotic mechanism.

bioRxiv · Dec 23, 2024 · PreprintCancer Biology

NLRP3-induced systemic inflammation controls the development of JAK2V617F mutant myeloproliferative neoplasms

Ruth-Miriam Koerber, Calvin Krollmann, Kevin Cieslak, Elisabeth Tregel, Maria L. Saenz, Tim H. Brümmendorf, Steffen Koschmieder, Martin Griesshammer, Ines Gütgemann, Conny K. Baldauf, Thomas Fischer, Peter Brossart, Carl Christian Kolbe, Eicke Latz, Dominik Wolf, Lino L. Teichmann

This study shows that NLRP3 inflammasome activation drives JAK2V617F mutant myeloproliferative neoplasms by promoting inflammation, platelet production, and fibrosis, and that its inhibition can reverse disease features.

bioRxiv · Mar 9, 2024Cancer Biology