Author

S. Kobold

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 Immunology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:human· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Research Focus:host-pathogen & immune response· 1

Frequent Co-Authors

A. Holtermann· 1 shared A. M. Mansilla· 1 shared A. Oener· 1 shared A. S. Lamort· 1 shared A. Zernecke-Madsen· 1 shared B. Ghesquiere· 1 shared C. Henning· 1 shared C. Schultheiss· 1 shared

Activity by Year

2020-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 12 mutual co-author links

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1 shared paperCancer Biology

A. Holtermann

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Mutation-specific CAR T cells as precision therapy for IGLV3-21R110 expressing high-risk chronic lymphocytic leukemia

F. Maerkl, C. Schultheiss, M. Ali, S.-S. Chen, L. Egli, J. Mietz, O. Chijoke, L. Paschold, S. Spajic, A. Holtermann, J. Doerr, S. Stock, I. Piseddu, D. Anz, M. Duehren-von Minden, , M. Binder

This study develops CAR T cells targeting a specific mutation in CLL to selectively kill cancer cells while sparing healthy B cells.

bioRxiv · Sep 29, 2023 · PreprintCancer Biology

HIF-1α-mediated mitochondrial-glycolytic reprogramming controls the transition of precursor to terminally exhausted T cells

H. Wu, X. Zhao, S. M. Hochrein, M. Eckstein, G. F. Gubert, K. Knoepper, A. M. Mansilla, A. Oener, R. Doucet-Ladeveze, W. Schmitz, B. Ghesquiere, S. Theurich, J. Dudek, G. Gasteiger, A. Zernecke-Madsen, , M. Vaeth

This study identifies HIF-1α-mediated metabolic reprogramming as a mechanism controlling the transition of precursor T cells to terminally exhausted T cells in chronic infections and cancer.

bioRxiv · Aug 31, 2023 · PreprintImmunology

An in vivo inflammatory loop potentiates KRAS blockade

K. A. Arendt, G. Ntaliarda, V. Armenis, D. Kati, C. Henning, G. Giotopoulou, M. A. Pepe, L. V. Klotz, A. S. Lamort, R. A. Hatz, S. Kobold, G. T. Stathopoulos

The paper shows that KRAS-mutant tumors rely on an inflammatory loop involving C-C-motif chemokine ligand 2/interleukin-1β signaling, making them resistant to KRAS inhibitors in vivo but responsive in certain transplant models.

bioRxiv · Apr 19, 2020Cancer Biology