Author

F. Grebien

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· 5

Signature Assays, Organisms & Methods

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Organism:human· 5 Approach:experimental assay· 4 Assay:bulk RNA-seq· 3 Research Focus:cancer & tumor microenvironment· 3 Approach:statistical model· 3 Research Focus:chromatin & epigenetic regulation· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1

Frequent Co-Authors

T. Eder· 3 shared C. Wagner· 2 shared E. Heyes· 2 shared H. A. Neubauer· 2 shared H. Sorger· 2 shared M. Dahlhoff· 2 shared M. Herling· 2 shared R. Fleck· 2 shared

Activity by Year

2020-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

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3 shared papersCancer Biology

T. Eder

Mutual co-authors in cluster

Author profile →

5 papers

Recent·Most cited

Small molecule STAT3/5 inhibitors exhibit therapeutic potential in acute myeloid leukemia and extra-nodal natural killer/T cell lymphoma

D. Pölöske, H. Sorger, A. Schönbichler, E. D. de Araujo, H. A. Neubauer, A. Orlova, S. H. Timonen, D. I. Abdallah, A. Ianevski, H. Kuusanmäki, M. Surbek, C. Wagner, T. Suske, M. L. Metzelder, M. Bergmann, , R. Moriggl

This study evaluates small molecule STAT3/5 inhibitors for treating AML and NKCL, showing growth arrest and synergy with existing therapies in vitro and in vivo.

bioRxiv · Oct 12, 2023 · PreprintCancer Biology

TET2 lesions enhance the aggressiveness of CEBPA-mutant AML by rebalancing GATA2 expression

E. Heyes, A. S. Wilhelmson, A. Wenzel, G. Manhart, T. Eder, M. B. Schuster, E. Rzepa, S. Pundhir, T. D'Altri, C. Gentil, M. Meggendorfer, J. Schwaller, T. Haferlach, F. Grebien, B. T. Porse

This study identifies GATA2 as a target of the CEBPA-TET2 mutational axis in AML, showing how TET2 lesions rebalance GATA2 expression and enhance disease aggressiveness.

bioRxiv · Mar 28, 2023Cancer Biology

STAT5 Gain-of-Function Variants Promote Precursor T-Cell Receptor Activation to Drive T-Cell Acute Lymphoblastic Leukemia

T. Suske, H. Sorger, F. Ruge, N. Prutsch, M. W. Zimmerman, T. Eder, B. Maurer, C. Wagner, S. Schoenefeldt, K. Spirk, A. Pichler, T. Pemovska, C. Schweicker, D. Poeloeske, D. Jungherz, , R. Moriggl

This study identifies STAT5 gain-of-function mutations as drivers of T-ALL by promoting pre-TCR signaling and shows therapeutic targeting potential with STAT3/5 or ZAP70 inhibitors.

bioRxiv · Dec 21, 2022 · PreprintCancer Biology

Biomolecular Condensation Drives Leukemia Caused by NUP98-Fusion Proteins

S. Terlecki-Zaniewicz, T. Eder, J. Schmoellerl, T. Humer, N. Kuchynka, K. Parapatics, E. Heyes, F. G. Liberante, A. C. Müller, F. Grebien

This study identifies biomolecular condensation as a mechanism by which NUP98-fusion proteins drive leukemia by altering condensate composition and gene regulation.

bioRxiv · Nov 16, 2020 · PreprintCancer Biology

Ablation of MYB-dependent leukaemia phenotype in MLL-driven AML correlates with increased expression of MAFB.

C. Ward, P. Cauchy, D. S. Walton, M. L. Clarke, D. Blakemore, F. Grebien, P. Garcia, J. Frampton, G. Volpe

The paper shows that MYB ablation in MLL-driven AML increases MAFB expression, while this effect is absent in AML with complex karyotypes.

bioRxiv · May 27, 2020 · PreprintCancer Biology