Author

E. J. Curtis

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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Approach:experimental assay· 3 Research Focus:cancer & tumor microenvironment· 2 Organism:human· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1 Assay:clinical cohort / trial· 1 Assay:DNA methylation· 1 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

P. S. Mischel· 3 shared J. Tang· 2 shared A. B. Pinkerton· 1 shared A. Khan· 1 shared A. M. Armando· 1 shared A. Rzhetsky· 1 shared A. Steffy· 1 shared B. Daniel· 1 shared

Activity by Year

2021-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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3 shared papersCancer Biology

P. S. Mischel

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Author profile →

3 papers

Recent·Most cited

Rampant transcription replication conflict creates therapeutic vulnerability in extrachromosomal DNA containing cancers

J. Tang, N. E. Weiser, G. Wang, S. Chowdhry, E. J. Curtis, Y. Zhao, I. T.-L. Wong, G. K. Marinov, R. Li, P. Hanoian, E. Tse, R. Hansen, J. Plum, A. Steffy, S. Milutinovic, , H. Y. Chang

This paper identifies transcription-replication conflict as a vulnerability in ecDNA-containing cancers and demonstrates that CHK1 inhibition selectively kills these tumors.

bioRxiv · Mar 29, 2024 · PreprintCancer Biology

Disparate pathways for extrachromosomal DNA biogenesis and genomic DNA repair

J. C. Rose, I. T.-L. Wang, B. Daniel, M. G. Jones, K. E. Yost, K. L. Hung, E. J. Curtis, P. S. Mischel, H. Chang

This study uses a CRISPR-based method to investigate ecDNA formation, showing efficient circularization and distinct repair pathways for ecDNA and chromosomal scars.

bioRxiv · Oct 22, 2023Cancer Biology

Targeting Glioblastoma Signaling and Metabolism with A Re-Purposed Brain-Penetrant Drug

J. Bi, A. Khan, J. Tang, S. Wu, W. Zhang, R. C. Gimple, T. Koga, A. M. Armando, S. Miki, H. Yang, B. Prager, E. J. Curtis, D. A. Wainwright, F. B. Furnari, J. N. Rich, , P. S. Mischel

This study identifies fluoxetine as a potential therapy for glioblastoma by inhibiting SMPD1 and enhancing temozolomide efficacy, with real-world evidence suggesting improved survival.

bioRxiv · Mar 16, 2021Cancer Biology