Author

M. E. Honeywell

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Cancer Biology· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Organism:human· 3 Approach:genetic perturbation / CRISPR· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Assay:CRISPR screen· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

M. J. Lee· 3 shared P. Cruz-Gordillo· 2 shared C. S. Fraser· 1 shared D. A. Guertin· 1 shared G. Ozcan· 1 shared J. B. Spinelli· 1 shared K. A. Sarosiek· 1 shared M. S. Isidor· 1 shared

Activity by Year

2020-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 31 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

3 shared papersCancer Biology

M. J. Lee

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Functional genomics reveals an off-target dependency of drug synergy in gastric cancer therapy

O. Leylek, M. E. Honeywell, M. J. Lee, M. T. Hemann, G. Ozcan

The paper identifies an off-target dependency of erlotinib in enhancing SN38's synergistic effect in gastric cancer through functional genomics.

bioRxiv · Oct 7, 2023Cancer Biology

p53 controls choice between apoptotic and non-apoptotic death following DNA damage

M. E. Honeywell, M. S. Isidor, N. W. Harper, R. E. Fontana, P. Cruz-Gordillo, S. A. Porto, C. S. Fraser, K. A. Sarosiek, D. A. Guertin, J. B. Spinelli, M. J. Lee

This study shows p53 regulates whether DNA damage triggers apoptosis or non-apoptotic death, revealing that p53-deficient cells die via MPT-driven necrosis due to high basal respiration.

bioRxiv · Jan 17, 2023 · PreprintCell Biology

ELP-dependent expression of MCL1 promotes resistance to EGFR inhibition in triple-negative breast cancer cells

P. Cruz-Gordillo, M. E. Honeywell, T. Leete, M. J. Lee

The study identifies the ELP complex as a mediator of resistance to EGFR inhibition in TNBC by promoting MCL1 expression, suggesting co-targeting EGFR and MCL1 as a therapeutic strategy.

bioRxiv · Mar 29, 2020Cancer Biology