Author

K. W. Mouw

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:cancer & tumor microenvironment· 2 Research Focus:gene regulatory network inference· 2 Approach:genetic perturbation / CRISPR· 2 Approach:statistical model· 2 Assay:bulk RNA-seq· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

Z. Szallasi· 3 shared A. S. Kibel· 2 shared C. Miao· 2 shared L. Jia· 2 shared T. Takai· 2 shared T. Tsujino· 2 shared T. Tsutsumi· 2 shared Z. Sztupinszki· 2 shared

Activity by Year

2021-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

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3 shared papersCancer Biology

Z. Szallasi

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Author profile →

3 papers

Recent·Most cited

Nucleotide excision repair deficiency is a targetable therapeutic vulnerability in clear cell renal cell carcinoma.

A. Prosz, H. Duan, V. Tisza, P. Sahgal, S. Topka, G. T.Klus, J. Borscok, Z. Sztupinszki, T. Hanlon, M. Diossy, L. Vizkeleti, D. R. Stormoen, I. Csabai, H. Pappot, J. Vijai, , Z. Szallasi

This paper identifies NER deficiency as a targetable vulnerability in ccRCC, showing that 10% of patients may respond to irofulven based on mutational signatures and PTGR1 expression.

bioRxiv · Feb 7, 2023Cancer Biology

CRISPR screens reveal genetic determinants of PARP inhibitor sensitivity and resistance in prostate cancer

T. Tsujino, T. Takai, K. Hinohara, F. Gui, T. Tsutsumi, X. Bai, C. Miao, C. Feng, B. Gui, S. Sztupinszki, A. Simoneau, N. Xie, L. Fazli, X. Dong, H. Azuma, , L. Jia

This study uses CRISPR screens to identify genetic factors affecting PARP inhibitor sensitivity and resistance in prostate cancer, revealing novel targets and mechanisms.

bioRxiv · Apr 13, 2022 · PreprintCancer Biology

RB1 loss overrides PARP inhibitor sensitivity driven by RNASEH2B loss in prostate cancer

c. Miao, T. Tsujino, T. Takai, G. Fu, T. Tsutsumi, Z. Sztupinszki, Z. Szallasi, K. W. Mouw, A. S. Kibel, L. Jia

The paper shows that loss of RNASEH2B makes prostate cancer cells sensitive to PARP inhibitors, but co-deletion with RB1 reduces this sensitivity through BRCA2 upregulation, and ATR inhibition can restore sensitivity.

bioRxiv · Nov 8, 2021Cancer Biology