Author

E. Compe

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 Cell Biology· 1

Signature Assays, Organisms & Methods

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Organism:human· 3 Assay:bulk RNA-seq· 2 Research Focus:differential expression· 2 Approach:experimental assay· 2 Research Focus:gene regulatory network inference· 2 Approach:statistical model· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1

Frequent Co-Authors

F. Coin· 3 shared g. davidson· 3 shared i. Davidson· 3 shared M. Cigrang· 3 shared P. Berico· 3 shared j.-m. egly· 2 shared M. Nogaret· 2 shared t. ye· 2 shared

Activity by Year

2020-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 43 mutual co-author links

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3 shared papersCancer Biology

F. Coin

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Novel synthetic ecteinascidins exhibit potent anti-melanoma activity by suppressing super-enhancer-driven oncogenic transcription

M. Cigrang, j. Obid, i. Davidson, M. Nogaret, t. ye, g. davidson, P. Catez, P. Berico, c. capelli, C. Marechal, A. Zachayus, C. Elly, T.-K. Li, E. Compe, P. Aviles, , F. Coin

This study shows novel synthetic ecteinascidins effectively treat melanoma by inhibiting super-enhancer-driven oncogenic transcription, even in resistant models.

bioRxiv · Mar 26, 2024 · PreprintCancer Biology

Super-enhancer driven expression of BAHCC1 promotes melanomacell proliferation and genome stability

P. Berico, M. Nogaret, G. Gambi, G. Davidson, M. Cigrang, B. Vokshi, S. Le Gras, G. Mengus, T. Ye, M. Dalmasso, E. Compe, C. Bertolotto, I. Davidson, F. Coin

The paper identifies BAHCC1 as a super-enhancer-driven gene in melanoma that promotes proliferation and genome stability, showing its potential as a therapeutic target.

bioRxiv · Jan 18, 2023Cancer Biology

TFIIH kinase CDK7 antagonizes phenotype switching and emergence of drug tolerance in melanoma

P. Berico, m. cigrang, C. Braun, G. Davidson, j. Sandoz, S. Legras, F. peyresaubes, C. G. Robles, j.-m. egly, e. compe, I. Davidson, F. Coin

The paper shows CDK7 inhibition causes melanoma cells to switch from a melanocytic to mesenchymal phenotype and develop drug tolerance through a GATA6-regulated gene program.

bioRxiv · Sep 24, 2020 · PreprintCell Biology