Author

W. Hahn

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· 6

Signature Assays, Organisms & Methods

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Organism:human· 6 Approach:statistical model· 5 Research Focus:drug response / drug discovery· 4 Approach:experimental assay· 4 Assay:bulk RNA-seq· 3 Research Focus:gene regulatory network inference· 3 Research Focus:differential expression· 2 Organism:mouse· 2

Frequent Co-Authors

D. E. Root· 3 shared J. S. Boehm· 3 shared A. Tsherniak· 2 shared F. Vazquez· 2 shared J. M. Dempster· 2 shared J. P. Rennhack· 2 shared A. A. Borah· 1 shared A. A. Salahudeen· 1 shared

Activity by Year

2018-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 20 mutual co-author links

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3 shared papersCancer Biology

D. E. Root

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6 papers

Recent·Most cited

Aberrant cell state plasticity mediated by developmental reprogramming precedescolorectal cancer initiation

P. Bala, J. P. Rennhack, D. Aitymbayev, C. X. Morris, S. M. Moyer, G. N. Duronio, P. Doan, z. Li, X. Liang, J. L. Hornick, M. B. Yurgelun, W. Hahn, N. S. Sethi

The paper shows that aberrant cell state plasticity, driven by regenerative activity and developmental reprogramming, occurs before colorectal cancer initiation in mouse models and human patients.

bioRxiv · Sep 22, 2022Cancer Biology

Partial gene suppression improves identification of cancer vulnerabilities when CRISPR-Cas9 knockout is pan-lethal

J. M. Krill-Burger, J. M. Dempster, A. A. Borah, B. R. Paolella, D. E. Root, T. R. Golub, J. S. Boehm, W. Hahn, J. M. McFarland, F. Vazquez, A. Tsherniak

This study compares CRISPR-Cas9 and RNAi screens to identify cancer vulnerabilities, finding that RNAi better detects pan-dependencies while CRISPR identifies more dependencies overall.

bioRxiv · Mar 2, 2022Cancer Biology

Pan-cancer organoid validation of tumor outlier chromosomal amplification events

A. A. Salahudeen, K. Yuki, J. Seoane, A. T. Mah, A. R. Smith, K. Kolahi, S. M. De la O, D. J. Hart, J. Ding, Z. Ma, S. A. Barkal, N. D. Shukla, H. C. Zhang, M. A. Cantrell, A. Batish, , C. J. Kuo

The paper validates oncogenic chromosomal amplification events across multiple cancers using organoid models and functional assays.

bioRxiv · Oct 5, 2021 · PreprintCancer Biology

CREB5 reprograms nuclear interactions to promote resistance to androgen receptor targeting therapies

J. H. Hwang, R. Arafeh, J.-H. Seo, S. C. Baca, M. Ludwig, T. E. Arnoff, C. Richter, H. E. Bergom, S. McSweeney, J. P. Rennhack, S. A. Klingenberg, A. T. Cheung, J. Kwon, J. So, S. Kregel, , W. Hahn

This study identifies CREB5 as a key driver of resistance to androgen receptor targeting therapies by reprogramming nuclear interactions and activating TGFβ and Wnt signaling pathways.

bioRxiv · Aug 18, 2021Cancer Biology

Gene expression has more power for predicting in vitro cancer cell vulnerabilities than genomics

J. M. Dempster, J. Krill-Burger, A. Warren, J. McFarland, J. S. Boehm, F. Vazquez, W. Hahn, T. Golub, A. Tsherniak

This study compares DNA- and expression-based models for predicting cancer cell viability and finds expression models are more accurate and interpretable.

bioRxiv · Feb 21, 2020 · PreprintCancer Biology

Renal medullary carcinomas depend upon SMARCB1 loss and are sensitive to proteasome inhibition

A. L. Hong, Y.-Y. Tseng, J. A. Wala, W. J. Kim, B. D. Kynnap, M. B. Doshi, G. Kugener, G. J. Sandoval, T. P. Howard, J. Li, X. Yang, M. Tillgren, M. Ghandi, A. Sayeed, R. Deasy, , W. Hahn

This study identifies SMARCB1 loss as critical for RMC survival and shows proteasome inhibition as a potential therapeutic strategy.

bioRxiv · Dec 5, 2018Cancer Biology