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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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Cell-Cycle Reprogramming for PI3K Inhibition Overrides a Relapse-Specific C481S BTK Mutation Revealed by Longitudinal Functional Genomics in Mantle Cell Lymphoma

TL;DR: The first relapse-specific BTK mutation is discovered in patients with MCL with acquired resistance, but not primary resistance, to ibrutinib, and a rationale for targeting the proliferative resistant MCL cells by inhibiting CDK4 and the cell cycle in combination with ibrUTinib in the presence of BTK(WT) or a PI3K inhibitor independent of BTk mutation is demonstrated.
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Whole-Exome Sequencing of Metastatic Cancer and Biomarkers of Treatment Response.

TL;DR: The majority of advanced, treatment-resistant tumors across tumor types harbor biologically informative alterations, and the establishment of a clinical trial for WES of metastatic tumors with prospective follow-up of patients can help identify candidate predictive biomarkers of response.
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Synergistic Activation of Inflammatory Cytokine Genes by Interferon-γ-Induced Chromatin Remodeling and Toll-like Receptor Signaling

TL;DR: This work found that IFN-γ induced sustained occupancy of transcription factors STAT1, IRF-1, and associated histone acetylation at promoters and enhancers at the TNF, IL6, and IL12B loci and provided a synergy mechanism whereby IFN -γ creates a primed chromatin environment to augment TLR-induced gene transcription.
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Flow Sorting and Exome Sequencing Reveal the Oncogenome of Primary Hodgkin and Reed-Sternberg Cells

TL;DR: In an extended cohort of 145 patients, the absence of B2M protein in the HRS cells was associated with lower stage of disease, younger age at diagnosis, and better overall and progression-free survival, suggesting that B 2M deficiency determines the tumor microenvironment and may define a major subset of cHL that has more uniform clinical and morphologic features.