Author

O. Witt

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· 4

Signature Assays, Organisms & Methods

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Organism:human· 4 Research Focus:cell type annotation· 3 Research Focus:differential expression· 3 Approach:statistical model· 3 Approach:deep learning· 2 Assay:scRNA-seq· 2 Assay:bulk RNA-seq· 1 Research Focus:clustering· 1

Frequent Co-Authors

S. M. Pfister· 4 shared A. Korshunov· 3 shared D. T. W. Jones· 3 shared A. Rademacher· 2 shared A. Wittmann· 2 shared B. Jones· 2 shared B. Statz· 2 shared C. M. van Tilburg· 2 shared

Activity by Year

2020-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 39 mutual co-author links

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4 shared papersCancer Biology

S. M. Pfister

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4 papers

Recent·Most cited

Cell-state plasticity drives heterogeneity in Group 3/4 medulloblastoma

P. Joshi, P. B. G. da Silva, K. Okonechnikov, T. Stelzer, I. Sarropoulos, M. Sepp, J. Nolle, M. V. Pour-Jamnani, A. Rademacher, T. Yamada, C. Schneider, J. Schmidt, L. Bianchini, P. Schaefer, K. Leiss, , L. M. Kutscher

This study identifies cell-state plasticity as a driver of heterogeneity in Group 3/4 medulloblastomas, showing that transcription factor perturbation can redirect tumor cells along different differentiation trajectories.

bioRxiv · Feb 9, 2024 · PreprintCancer Biology

Medulloblastoma oncogene aberrations are not involved in tumor initiation, but essential for disease progression and therapy resistance

K. Okonechnikov, P. Joshi, V. Koerber, A. Rademacher, M. Bortolomeazzi, J.-P. Mallm, P. B. G. da Silva, B. Statz, M. Sepp, I. Sarropoulos, T. Yamada-Saito, J. Vaillant, A. Wittmann, K. Schramm, M. Blattner-Johnson, , S. M. Pfister

The paper uses single-cell technologies to show that large-scale chromosomal aberrations drive medulloblastoma initiation, while single-gene oncogenic events like MYC contribute to progression and therapy resistance.

bioRxiv · Feb 9, 2024Cancer Biology

Chromosome 8 gain drives cancer progression by hijacking the translation factor 4E-BP1 sensitizing for targeted CDK4/6 inhibition

C. M. Funk, A. Ehlers, M. F. Orth, K. Aljakouch, J. Li, T. L. B. Hoelting, R. Will, A. K. Ceranski, F. Willis, E. Vinca, S. Ohmura, R. Imle, J. Siebenlist, A. Yershova, M. M. L. Knott, , J. Musa

This study identifies chr8 gains and 4E-BP1 expression as prognostic markers in Ewing sarcoma, showing they drive cancer progression by promoting proliferation and sensitizing to CDK4/6 inhibitors.

bioRxiv · Dec 11, 2022 · PreprintCancer Biology

A subset of pediatric thalamic gliomas share a distinct DNA methylation profile, H3K27me3 loss and frequent alteration of EGFR

P. Sievers, M. Sill, D. Schrimpf, D. Stichel, D. E. Reuss, D. Sturm, J. Hench, S. Frank, L. Krskova, A. Vicha, M. Zapotocky, B. Bison, P. N. Harter, M. Snuderl, C. M. Kramm, , F. Sahm

This study identifies a distinct subset of pediatric gliomas with EGFR alterations, H3K27me3 loss, and broad tumor localization, suggesting EGFR inhibition as a potential therapy.

bioRxiv · Aug 28, 2020Cancer Biology