Author

E. Keung

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· 1 Research Focus:cell type annotation· 1 Assay:ChIP-seq· 1 Research Focus:differential expression· 1 Approach:experimental assay· 1 Organism:human· 1 Organism:mouse· 1 Approach:statistical model· 1

Frequent Co-Authors

A. Lazar· 2 shared C. Terranova· 2 shared K. Rai· 2 shared M. Maitituoheti· 2 shared M. Tang· 2 shared S. Jiang· 2 shared S. Sarkar· 2 shared A. Chaudhri· 1 shared

Activity by Year

2018-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 43 mutual co-author links

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2 shared papersCancer Biology

A. Lazar

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2 papers

Recent·Most cited

Enhancer Reprogramming in Melanoma Immune Checkpoint Therapy Resistance

M. Maitituoheti, A. Shi, M. Tang, L.-L. Ho, C. Terranova, K. Galani, E. Keung, C. Creasy, M. Wu, J. Chen, N. Chen, A. Singh, A. Chaudhri, N. Anvar, G. Tarantino, , K. Rai

The paper identifies enhancer-based biomarkers of resistance to anti-PD-1 therapy in melanoma and suggests enhancer blockade combined with ICB as a potential strategy to improve treatment responses.

bioRxiv · Aug 31, 2022 · PreprintCancer Biology

Enhancer Reprogramming Confers Dependence on Glycolysis and IGF signaling in KMT2D Mutant Melanoma

M. Maitituoheti, E. Keung, M. Tang, L. Yan, H. Alam, G. Han, A. Raman, C. Terranova, S. Sarkar, E. Orouji, S. Amin, S. Sharma, M. Williams, N. S. Samant, M. Dhamdhere, , K. Rai

This study identifies KMT2D as a tumor suppressor in melanoma, showing its loss leads to metabolic reprogramming toward glycolysis and dependence on IGF signaling, suggesting therapeutic targeting of these pathways.

bioRxiv · Dec 27, 2018Cancer Biology