Author

K. Bowland

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· 4

Signature Assays, Organisms & Methods

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Organism:human· 4 Research Focus:cancer & tumor microenvironment· 3 Approach:genetic perturbation / CRISPR· 3 Assay:whole-genome sequencing· 2 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:drug response / drug discovery· 1 Research Focus:gene regulatory network inference· 1 Approach:statistical model· 1

Frequent Co-Authors

A. Skaist· 3 shared J. R. Eshleman· 3 shared N. J. Roberts· 3 shared R. H. Hruban· 3 shared S. S. K. Teh· 3 shared A. Bennett· 2 shared E. Halper-Stromberg· 2 shared H. Liang· 2 shared

Activity by Year

2022-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 41 mutual co-author links

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3 shared papersCancer Biology

A. Skaist

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Author profile →

4 papers

Recent·Most cited

Islands of genomic stability in the face of genetically unstable metastatic cancer

K. Bowland, J. Lai, A. Skaist, Y. Zhang, S. S. K. Teh, N. J. Roberts, E. Thompson, S. J. Wheelan, R. H. Hruban, R. Karchin, C. A. Iacobuzio-Donahue, J. R. Eshleman

The paper identifies genomically stable regions in metastatic pancreatic cancer that can be targeted by CRISPR-Cas9 due to preserved PAM sites, suggesting a potential gene therapy approach.

bioRxiv · Jan 26, 2024Cancer Biology

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

S. S. K. Teh, K. Bowland, A. Bennett, E. Halper-Stromberg, A. Skaist, J. Tang, F. Cai, A. Macoretta, H. Liang, H. Kamiyama, S. Wheelan, M.-T. Lin, R. H. Hruban, R. B. Scharpf, N. J. Roberts, 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.

bioRxiv · Apr 15, 2023Cancer Biology

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

S. S. K. Teh, A. Kotwal, A. Bennett, E. Halper-Stromberg, L. Morsberger, S. Zamani, Y. Shi, A. Skaist, Q. Zhu, K. Bowland, H. Liang, R. H. Hruban, C.-F. Hung, R. A. Anders, N. J. Roberts, , 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.

bioRxiv · Apr 3, 2023Cancer Biology

Collateral lethality between HDAC1 and HDAC2 exploits cancer-specific NuRD complex vulnerabilities

Y. Zhang, D. Remillard, U. Onubogu, B. Karakyriakou, J. N. Asiaban, A. R. Ramos, K. Bowland, T. R. Bishop, C. J. Ott, M. Janiszewska, B. F. Cravatt, M. A. Erb

The paper identifies collateral synthetic lethality between HDAC1 and HDAC2 in cancer cells and shows that targeting HDAC2 can suppress tumor growth by disrupting the NuRD complex.

bioRxiv · May 30, 2022Cancer Biology