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William G. Nelson

Researcher at Johns Hopkins University School of Medicine

Publications -  302
Citations -  32149

William G. Nelson is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Prostate cancer & Prostate. The author has an hindex of 93, co-authored 292 publications receiving 30356 citations. Previous affiliations of William G. Nelson include New York University & Johns Hopkins University.

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Epigenetic DNA methylation of antioxidative stress regulator NRF2 in human prostate cancer.

TL;DR: It is suggested that epigenetic modification may contribute to the regulation of transcription activity of NRF2, which could be used as prevention and treatment target of human prostate cancer.
Journal Article

Specific Keratins as Molecular Markers for Neoplasms with a Stratified Epithelial Origin

TL;DR: The results suggest that the Mr 50,000 and 58,000 keratins provide useful molecular markers for identifying neoplasms of stratified squamous epithelial origin.
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Detection of GSTP1 methylation in prostatic secretions using combinatorial MSP analysis.

TL;DR: Genomic DNA with GSTP1 promoter methylation can be detected in prostatic secretion specimens from the great majority of men with localized prostate cancer and may serve as useful adjuncts to existing methods for prostate cancer screening and prognostication.
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Chromosome-wide mapping of DNA methylation patterns in normal and malignant prostate cells reveals pervasive methylation of gene-associated and conserved intergenic sequences

TL;DR: Comparison of chromosome-wide DNA methylation patterns in normal and malignant prostate cells revealed significant methylation of gene-proximal and conserved intergenic sequences and can be easily extended for genome-wide methylation analysis in health and disease.
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Androgen ablation-induced programmed death of prostatic glandular cells does not involve recruitment into a defective cell cycle or p53 induction.

TL;DR: It is demonstrated that prostatic glandular cells undergo programmed death in G(0) without recruitment into the G1 phase of a defective cell cycle, and that an increase in p53 protein or its function is not involved in this death process.