Author

s. gadal

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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Approach:experimental assay· 2 Organism:human· 2 Research Focus:cancer & tumor microenvironment· 1 Assay:DNA methylation· 1 Research Focus:drug response / drug discovery· 1 Assay:proteomics· 1 Assay:whole-exome sequencing· 1

Frequent Co-Authors

J. A. Boyer· 2 shared M. Sharma· 2 shared N. Rosen· 2 shared Q. Chang· 2 shared A. Barlas· 1 shared C. Amor· 1 shared D. Warner· 1 shared E. Chan· 1 shared

Activity by Year

2023-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 36 mutual co-author links

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2 shared papersCancer Biology

J. A. Boyer

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2 papers

Recent·Most cited

eIF4A controls translation of estrogen receptor alpha and is a therapeutic target in advanced breast cancer

J. A. Boyer, M. Sharma, M. Dorso, N. Mai, C. Amor, J. M. Reiter, R. Kannan, S. Gadal, J. Xu, M. Miele, L. Zhuoning, X. Chen, Q. Chang, F. Pareja, S. Worland, , N. Rosen

This paper identifies eIF4A as a key regulator of ER translation in breast cancer and shows that inhibiting eIF4A, either alone or with fulvestrant, suppresses ER expression and tumor growth in advanced ER+ breast cancer.

bioRxiv · May 8, 2024Cancer Biology

Tumorigenesis driven by the BRAF V600E oncoprotein requires secondary mutations that overcome its feedback inhibition of migration and invasion

s. gadal, J. A. Boyer, S. F. Roy, N. A. Outmezguine, M. Sharma, H. Li, N. Fan, E. Chan, Y. Romin, A. Barlas, Q. Chang, P. Pancholi, N. M. Timaul, M. Overholtzer, R. Yaeger, , N. Rosen

This study shows that BRAFV600E mutations inhibit cell migration and invasion through feedback inhibition of RAC1, requiring secondary mutations to overcome this block and enable tumorigenesis.

bioRxiv · Nov 21, 2023 · PreprintCancer Biology