Author

T. Veith

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 Microbiology· 1

Signature Assays, Organisms & Methods

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Organism:human· 3 Research Focus:cell type annotation· 2 Approach:statistical model· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:clustering· 1 Approach:experimental assay· 1 Research Focus:host-pathogen & immune response· 1 Assay:multiome· 1

Frequent Co-Authors

N. Andor· 2 shared A. Balazs· 1 shared A. C. Hocke· 1 shared A. M. Forero Pinto· 1 shared A. P. Gomes· 1 shared A. Richter· 1 shared A. Schultz· 1 shared B. Tenner· 1 shared

Activity by Year

2021-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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2 shared papersCancer Biology

N. Andor

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Interactions between ploidy and resource availability shape clonal interference at initiation and recurrence of glioblastoma

Z. Nowicka, F. Rentzeperis, R. Beck, V. Tagal, A. M. Forero Pinto, E. Scanu, T. Veith, J. Cole, D. Ilter, W. Dominguez Viqueira, J. K. Teer, K. Maksin, S. Pasetto, M. A. Abdalah, G. Fiandaca, , N. Andor

This study uses a mathematical model to show that ploidy and resource availability in the tumor microenvironment influence glioblastoma initiation and recurrence.

bioRxiv · Oct 17, 2023 · PreprintCancer Biology

Intra-tumor heterogeneity, turnover rate and karyotype space shape susceptibility to missegregation-induced extinction

G. J. Kimmel, R. J. Beck, X. Yu, T. Veith, S. Bakhoum, P. M. Altrock, N. Andor

The paper models chromosome missegregation in tumors to assess extinction risk, finding that intra-tumor heterogeneity and karyotype stability prevent extinction unless turnover rates are extremely high.

PLOS Computational Biology · Jan 23, 2023Peer-reviewedCancer Biology

Post-entry, spike-dependent replication advantage of B.1.1.7 and B.1.617.2 over B.1 SARS-CoV-2 in an ACE2-deficient human lung cell line

D. Niemeyer, S. Schroeder, K. Friedmann, F. Weege, J. Trimpert, A. Richter, S. Stenzel, J. Jansen, J. Emanuel, J. Kazmierski, F. Pott, L. M. Jeworowski, R. Olmer, M.-C. Jaboreck, B. Tenner, , C. Drosten

The paper shows that B.1.1.7 and B.1.617.2 SARS-CoV-2 variants have a replication advantage over B.1 in ACE2-deficient lung cells, suggesting reliance on alternative cellular factors.

bioRxiv · Oct 20, 2021 · PreprintMicrobiology