E
Etienne Dardenne
Researcher at Cornell University
Publications - 15
Citations - 1357
Etienne Dardenne is an academic researcher from Cornell University. The author has contributed to research in topics: Prostate cancer & Alternative splicing. The author has an hindex of 11, co-authored 13 publications receiving 991 citations. Previous affiliations of Etienne Dardenne include University of Paris & French Institute of Health and Medical Research.
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Journal ArticleDOI
N-Myc Induces an EZH2-Mediated Transcriptional Program Driving Neuroendocrine Prostate Cancer
Etienne Dardenne,Himisha Beltran,Matteo Benelli,Kaitlyn Gayvert,Adeline Berger,Loredana Puca,Joanna Cyrta,Andrea Sboner,Zohal Noorzad,Theresa Y. MacDonald,Cynthia Cheung,Ka Shing Yuen,Dong Gao,Yu Chen,Martin Eilers,Juan Miguel Mosquera,Juan Miguel Mosquera,Brian D. Robinson,Brian D. Robinson,Olivier Elemento,Mark A. Rubin,Francesca Demichelis,David S. Rickman,David S. Rickman +23 more
TL;DR: In this article, a genetically engineered mouse model and human prostate cancer transcriptome data were integrated to show that N-Myc overexpression leads to the development of poorly differentiated, invasive prostate cancer that is molecularly similar to human NEPC.
Journal ArticleDOI
RNA helicases DDX5 and DDX17 dynamically orchestrate transcription, miRNA, and splicing programs in cell differentiation.
Etienne Dardenne,Micaela Polay Espinoza,Laurent Fattet,Sophie Germann,Marie-Pierre Lambert,Helen Neil,Eleonora Zonta,Hussein Mortada,Lise Gratadou,Mathieu Deygas,Fatima Zahra Chakrama,Samaan Samaan,François-Olivier Desmet,Léon-Charles Tranchevent,Martin Dutertre,Ruth Rimokh,Cyril F. Bourgeois,Didier Auboeuf +17 more
TL;DR: A mechanism by which DDX5 and DDX17 cooperate with heterogeneous nuclear ribonucleoprotein H/F splicing factors to define epithelial- and myoblast-specific splicing subprograms is uncovered and it is proposed to name these proteins "master orchestrators of differentiation that dynamically orchestrate several layers of gene expression.
Journal ArticleDOI
A Phase II Trial of the Aurora Kinase A Inhibitor Alisertib for Patients with Castration-resistant and Neuroendocrine Prostate Cancer: Efficacy and Biomarkers
Himisha Beltran,Himisha Beltran,Clara Oromendia,Daniel C. Danila,Daniel C. Danila,Bruce Montgomery,Christopher J. Hoimes,Russell Z. Szmulewitz,Ulka N. Vaishampayan,Andrew J. Armstrong,Mark N. Stein,Jacek Pinski,Juan Miguel Mosquera,Juan Miguel Mosquera,Verena Sailer,Rohan Bareja,Alessandro Romanel,Naveen Gumpeni,Andrea Sboner,Andrea Sboner,Etienne Dardenne,Loredana Puca,Loredana Puca,Davide Prandi,Mark A. Rubin,Mark A. Rubin,Howard I. Scher,Howard I. Scher,David S. Rickman,David S. Rickman,Francesca Demichelis,Francesca Demichelis,David M. Nanus,David M. Nanus,Karla V. Ballman,Scott T. Tagawa,Scott T. Tagawa +36 more
TL;DR: Although the study did not meet its primary endpoint, a subset of patients with advanced prostate cancer and molecular features supporting Aurora-A and N-myc activation achieved significant clinical benefit from single-agent alisertib.
Journal ArticleDOI
Cotranscriptional exon skipping in the genotoxic stress response
Martin Dutertre,Gabriel Sanchez,Marie-Cécile De Cian,Marie-Cécile De Cian,Jérôme Barbier,Etienne Dardenne,Lise Gratadou,Gwendal Dujardin,Catherine Le Jossic-Corcos,Laurent Corcos,Didier Auboeuf +10 more
TL;DR: Genotoxic stress-induced alteration of the communication between the transcriptional and splicing machineries results in widespread exon skipping and plays a central role in the genot toxic stress response.
Journal ArticleDOI
Splicing switch of an epigenetic regulator by RNA helicases promotes tumor-cell invasiveness
Etienne Dardenne,Sandra Pierredon,Keltouma Driouch,Lise Gratadou,Magali Lacroix-Triki,Micaela Polay Espinoza,Eleonora Zonta,Sophie Germann,Hussein Mortada,Jean-Philippe Villemin,Martin Dutertre,Rosette Lidereau,Stéphan Vagner,Didier Auboeuf +13 more
TL;DR: It is shown that macroH2A1 splicing isoforms differentially regulate the transcription of a set of genes involved in redox metabolism, and reveals a new regulatory pathway in which splicing factors control the expression of histone variant isoforms that in turn drive a transcription program to switch tumor cells to an invasive phenotype.