Author

J. R. Eshleman

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

Signature Assays, Organisms & Methods

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Research Focus:cancer & tumor microenvironment· 2 Approach:genetic perturbation / CRISPR· 2 Organism:human· 2 Assay:whole-genome sequencing· 1

Frequent Co-Authors

A. Bennett· 2 shared A. Skaist· 2 shared E. Halper-Stromberg· 2 shared H. Liang· 2 shared K. Bowland· 2 shared N. J. Roberts· 2 shared R. B. Scharpf· 2 shared R. H. Hruban· 2 shared

Activity by Year

2023-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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2 shared papersCancer Biology

A. Bennett

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2 papers

Recent·Most cited

Cancer BiologybioRxivApr 15, 2023

CRISPR-Cas9 for selective targeting of somatic mutations in pancreatic cancers

S. S. K. Teh, K. Bowland, A. Bennett…·J. R. Eshleman

This paper demonstrates CRISPR-Cas9 can selectively target somatic mutations in pancreatic cancer by exploiting PAMs in noncoding regions, achieving >80% cell death with minimal off-target effects.

DOI 10.1093/narcan/zcae028

humanwhole-genome sequencing

𝕏 PostBluesky

Cancer BiologybioRxivApr 3, 2023

Simultaneous CRISPR-Cas9-induced double strand breaks are lethal in models of pancreatic cancer

S. S. K. Teh, A. Kotwal, A. Bennett…·J. R. Eshleman

This study shows CRISPR-Cas9-induced DNA double-strand breaks are more cytotoxic to pancreatic cancer cells than radiation-induced breaks, with significant tumor growth inhibition and chromosomal instability.

DOI 10.1172/jci190121

humangenetic perturbation / CRISPR

𝕏 PostBluesky