Author

C. Vaziri

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· 3

Signature Assays, Organisms & Methods

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Organism:human· 3 Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Assay:DNA methylation· 2 Research Focus:gene regulatory network inference· 2 Approach:genetic perturbation / CRISPR· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1

Frequent Co-Authors

D. Wu· 2 shared J. An· 2 shared Y. Gao· 2 shared Y. Yang· 2 shared A. B. Satterlee· 1 shared A. Fradet-Turcotte· 1 shared A. Jablonski· 1 shared A. Shelton· 1 shared

Activity by Year

2021-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 35 mutual co-author links

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2 shared papersCancer Biology

D. Wu

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Author profile →

3 papers

Recent·Most cited

The DNA Damage Response (DDR) landscape of endometrial cancer defines discrete disease subtypes and reveals therapeutic opportunities.

X. Zhang, S. Joseph, D. Wu, J. Bowser, C. Vaziri

This study characterizes DDR and CTA transcriptional landscapes in endometrial cancer subtypes, identifies aggressive subtypes, and reveals therapeutic vulnerabilities.

bioRxiv · Nov 20, 2023Cancer Biology

Trans-Lesion Synthesis and Mismatch Repair Pathway Crosstalk Defines Chemoresistance and Hypermutation Mechanisms in Glioblastoma

X. Cheng, J. An, J. Lou, Q. Gu, W. Ding, G. Droby, Y. Wang, C. Wang, Y. Gao, A. Shelton, A. B. Satterlee, B. E. Mann, Y.-C. Hsiao, C.-W. Liu, K. Liu, , Y. Yang

This study identifies RAD18's role in TMZ resistance and hypermutation in GBM by linking it to TLS and MMR pathways through CRISPR screening and mutation analysis.

bioRxiv · Oct 16, 2023 · PreprintCancer Biology

A Degenerate PCNA-Interacting Peptide (DPIP) box targets RNF168 to replicating DNA to limit 53BP1 signaling

Y. Yang, D. Jayaprakash, R. Hollingworth, S. Chen, A. Jablonski, E. Mutter-Rottmayer, Y. Gao, J. Anand Ramlal, J. An, X. Chen, K. Pearce, S.-A. Blanchet, A. Fradet-Turcotte, G. Stewart, C. Vaziri

This study identifies a non-canonical role of RNF168 at DNA replication forks, showing it suppresses 53BP1 signaling through PCNA binding, independent of its canonical DSB response function.

bioRxiv · Mar 17, 2021 · PreprintCancer Biology