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Olivier Elemento
Researcher at Cornell University
Publications - 596
Citations - 38936
Olivier Elemento is an academic researcher from Cornell University. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 82, co-authored 471 publications receiving 27739 citations. Previous affiliations of Olivier Elemento include Princeton University & Max Planck Society.
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Journal ArticleDOI
Divergent clonal evolution of castration-resistant neuroendocrine prostate cancer
Himisha Beltran,Himisha Beltran,Davide Prandi,Juan Miguel Mosquera,Juan Miguel Mosquera,Matteo Benelli,Loredana Puca,Joanna Cyrta,Clarisse Marotz,Eugenia G. Giannopoulou,Balabhadrapatruni V. S. K. Chakravarthi,Sooryanarayana Varambally,Scott A. Tomlins,David M. Nanus,Scott T. Tagawa,Eliezer M. Van Allen,Eliezer M. Van Allen,Olivier Elemento,Olivier Elemento,Andrea Sboner,Andrea Sboner,Levi A. Garraway,Levi A. Garraway,Levi A. Garraway,Mark A. Rubin,Mark A. Rubin,Francesca Demichelis,Francesca Demichelis,Francesca Demichelis +28 more
TL;DR: Analysis of whole-exome sequencing data of metastatic biopsies from patients observed substantial genomic overlap between castration-resistant tumors that were histologically characterized as prostate adenocarcinomas and neuroendocrine prostate cancer (CRPC-NE), supporting the emergence of an alternative, 'AR-indifferent' cell state through divergent clonal evolution as a mechanism of treatment resistance in advanced prostate cancer.
Journal ArticleDOI
Chromosomal instability drives metastasis through a cytosolic DNA response.
Samuel F. Bakhoum,Samuel F. Bakhoum,Bryan Ngo,Ashley M. Laughney,Julie Ann Cavallo,Julie Ann Cavallo,Charles J. Murphy,Peter Ly,Pragya Shah,Roshan K. Sriram,Thomas B.K. Watkins,Neil K. Taunk,Mercedes Duran,Mercedes Duran,Chantal Pauli,Christine Shaw,Kalyani Chadalavada,Vinagolu K. Rajasekhar,Giulio Genovese,Subramanian Venkatesan,Nicolai Juul Birkbak,Nicholas McGranahan,Mark R. Lundquist,Quincey LaPlant,John H. Healey,Olivier Elemento,Christine H. Chung,Nancy Y. Lee,Marcin Imielenski,Gouri Nanjangud,Dana Pe'er,Don W. Cleveland,Simon N. Powell,Jan Lammerding,Charles Swanton,Lewis C. Cantley +35 more
TL;DR: It is shown that chromosomally unstable tumour cells co-opt chronic activation of innate immune pathways to spread to distant organs by sustaining a tumour cell-autonomous response to cytosolic DNA.
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Reversible methylation of m6Am in the 5′ cap controls mRNA stability
Jan Mauer,Xiaobing Luo,Alexandre Blanjoie,Xinfu Jiao,Anya V. Grozhik,Deepak P. Patil,Bastian Linder,Brian F. Pickering,Jean-Jacques Vasseur,Qiuying Chen,Steven S. Gross,Olivier Elemento,Françoise Debart,Megerditch Kiledjian,Samie R. Jaffrey +14 more
TL;DR: Using a transcriptome-wide map of m6Am, it is found that m 6Am-initiated transcripts are markedly more stable than mRNAs that begin with other nucleotides and that m6 am is selectively demethylated by fat mass and obesity-associated protein (FTO).
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EZH2 Is Required for Germinal Center Formation and Somatic EZH2 Mutations Promote Lymphoid Transformation
Wendy Béguelin,Relja Popovic,Matt Teater,Yanwen Jiang,Karen L. Bunting,Monica Rosen,Hao Shen,Shao Ning Yang,Ling Wang,Teresa Ezponda,Eva Martinez-Garcia,Haikuo Zhang,Yupeng Zheng,Sharad K. Verma,Michael T. McCabe,Heidi M. Ott,Glenn S. Van Aller,Ryan G. Kruger,Yan Liu,Charles F. McHugh,David Scott,Young Rock Chung,Neil L. Kelleher,Rita Shaknovich,Caretha L. Creasy,Randy D. Gascoyne,Kwok-Kin Wong,Leandro Cerchietti,Ross L. Levine,Omar Abdel-Wahab,Jonathan D. Licht,Olivier Elemento,Ari Melnick +32 more
TL;DR: GC B cell (GCB)-type diffuse large B cell lymphomas (DLBCLs) are mostly addicted to EZH2 but not the more differentiated activated B cell(ABC)-type DLBCLS, thus clarifying the therapeutic scope of EZh2 targeting.
Journal ArticleDOI
Vitamin C selectively kills KRAS and BRAF mutant colorectal cancer cells by targeting GAPDH
Jihye Yun,Edouard Mullarky,Edouard Mullarky,Changyuan Lu,Kaitlyn Bosch,Adam Kavalier,Keith Rivera,Jatin Roper,Iok In Christine Chio,Eugenia G. Giannopoulou,Carlo Rago,Ashlesha Muley,John M. Asara,Jihye Paik,Olivier Elemento,Zhengming Chen,Darryl J. Pappin,Lukas E. Dow,Nickolas Papadopoulos,Steven S. Gross,Lewis C. Cantley +20 more
TL;DR: It is found that cultured human CRC cells harboring KRAS or BRAF mutations are selectively killed when exposed to high levels of vitamin C, due to increased uptake of the oxidized form of Vitamin C, dehydroascorbate (DHA), via the GLUT1 glucose transporter.