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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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The Role of Next-Generation Sequencing in Precision Medicine: A Review of Outcomes in Oncology

TL;DR: The early findings of the impact of next-generation sequencing on cancer patient outcomes are discussed and increased transparency around the determination of “actionable mutations” and a heightened focus on investigating the variations in health insurance coverage across patients receiving sequencing-matched therapies are recommended.
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Histone variant H3.3 is an essential maternal factor for oocyte reprogramming.

TL;DR: H3.3 is a crucial maternal factor for oocyte reprogramming and provides a practical model to directly dissect the oocyte for its reprograming capacity, and can be rescued by injecting exogenous H3.2 mRNA into oocytes in SCNT embryos.
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R-Spondin chromosome rearrangements drive Wnt-dependent tumour initiation and maintenance in the intestine

TL;DR: This study provides direct evidence that endogenous Rspo2 and RSPo3 chromosome rearrangements can initiate and maintain tumour development, and indicates a viable therapeutic window for LGK974 treatment of RSPO-fusion cancers.
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Revisiting the initial steps of sexual development in the malaria parasite Plasmodium falciparum.

TL;DR: In this paper, the authors used PfAP2-G, the master regulator of sexual conversion, as a marker of commitment in the early stages of the malaria life cycle and found that sexual conversion can occur by two different routes: the previously described route in which PfAP-G-expressing parasites complete a replicative cycle as committed forms before converting into gametocytes upon re-invasion, or a direct route with conversion within the same cycle as initial PfAP 2-G expression.
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AID stabilizes stem-cell phenotype by removing epigenetic memory of pluripotency genes

TL;DR: It is shown that Aid-null cells are transiently hyper-responsive to the reprogramming process, and hypermethylated genes associated with pluripotency fail to be stably upregulated, including many MYC target genes.