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Peter S. Nelson

Researcher at Fred Hutchinson Cancer Research Center

Publications -  497
Citations -  57568

Peter S. Nelson is an academic researcher from Fred Hutchinson Cancer Research Center. The author has contributed to research in topics: Prostate cancer & Cancer. The author has an hindex of 96, co-authored 425 publications receiving 47923 citations. Previous affiliations of Peter S. Nelson include University of Washington & National Institutes of Health.

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Biochemical properties of purified human retinol dehydrogenase 12 (RDH12) : Catalytic efficiency toward retinoids and C9 aldehydes and effects of cellular retinol-binding protein type I (CRBPI) and cellular retinaldehyde-binding protein (CRALBP) on the oxidation and reduction of retinoids

TL;DR: Tissue distribution of RDH12 and its catalytic properties suggest that, in most tissues,RDH12 primarily contributes to the reduction of all-trans-retinaldehyde; however, at saturating concentrations of peroxidic aldehydes in the cells undergoing oxidative stress, for example, photoreceptors, RDH 12 might also play a role in detoxification of lipid peroxidation products.
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ERG Activates the YAP1 Transcriptional Program and Induces the Development of Age-Related Prostate Tumors

TL;DR: It is determined that ERG activates the transcriptional program regulated by YAP1 of the Hippo signaling pathway and found that prostate-specific activation of either ERG or Yap1 in mice induces similar transcriptional changes and results in age-related prostate tumors.
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Toll receptors: an expanding role in our understanding of human disease.

TL;DR: Toll receptor proteins in Drosophila are involved in establishing the dorsal‐ventral axis in embryogenesis as well as participating in the innate immune response to invading pathogens, and a better understanding of this response may provide improved therapeutic modalities in the treatment of bacterial and fungal sepsis.
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Castration-resistant prostate cancer: Targeting androgen metabolic pathways in recurrent disease

TL;DR: It is indicated that prostate cancers undergo an adaptive response to castration that is associated with the up-regulation of transcripts encoding enzymes involved in the biosynthesis of androgens, and targeting these metabolic enzymes either individually or using combinations of agents to inhibit testicular, adrenal, and intracrine sources may provide enhanced clinical responses.