Author

Li Zhang

Institute for Research in Immunology and CancerORCID 0009-0001-8476-3536Unclaimed ORCID profile · follow to get notified of new preprints

Additional preprints under this name without ORCID

Li Zhang30 papers · Johns Hopkins University

Biology Disciplines

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Cancer Biology· 1 Genetics· 1 Systems Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Assay:CRISPR screen· 2 Research Focus:drug response / drug discovery· 2 Organism:human· 2 Approach:statistical model· 2 Research Focus:benchmarking· 1 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1

Frequent Co-Authors

Andrew Chatr‐aryamontriiD· 3 shared Thierry BertomeuiD· 3 shared Brian T. WilhelmiD· 2 shared Ivan TopisirovićiD· 2 shared Mike TyersiD· 2 shared Philippe P. RouxiD· 2 shared Sylvie MaderiD· 2 shared Vincent ArchambaultiD· 2 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 38 mutual co-author links

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3 shared papersSystems Biology

Andrew Chatr‐aryamontriORCID

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3 papers

Recent·Most cited

Systems BiologybioRxivPreprintJan 30, 2026

A Chemical-Genetic Interaction Matrix Reveals Drug Mechanism and Genetic Architecture

Jasmin Coulombe‐Huntington, Thierry Bertomeu, Caroline Huard…·Mike Tyers

The paper presents a chemical-genetic interaction matrix derived from CRISPR/Cas9 screens, revealing drug mechanisms and genetic architecture in human cells.

1 citation

humanCRISPR screen

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GeneticsbioRxivPreprintAug 4, 2025

A platform for the systematic interrogation of genetic interactions in human cells: 26 gene by genome-wide double knockout screens as a proof of concept

Andrew Chatr‐aryamontri, Li Zhang, Ndeye Khady Thiombane…·Thierry Bertomeu

The paper introduces a method for systematically studying genetic interactions in human cells using CRISPR/Cas9 screens and demonstrates its effectiveness through 26 gene by genome-wide knockout screens.

DOI 10.1101/2025.08.04.665369

humanCRISPR screen

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Cancer BiologybioRxivPreprintAug 3, 2025

On-target toxicity limits the efficacy of CDK11 inhibition against cancers with 1p36 deletions

Linda Julian, Lisa Crozier, Devon A. Lukow…·Jason M. Sheltzer

This study shows CDK11 is critical for cancer cell survival and identifies 1p36 deletions as a biomarker for CDK11 inhibitor sensitivity, but on-target toxicity limits therapeutic efficacy.

5 citations

mousebulk RNA-seq

𝕏 PostBluesky