W
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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Journal ArticleDOI
The molecular pathogenesis of prostate cancer: Implications for prostate cancer prevention
TL;DR: A hypothesized critical role for GSTP1 inactivation in the earliest steps of prostatic carcinogenesis provides several attractive opportunities for prostate cancer prevention strategies, including restoration of GSTP 1 function, compensation for inadequate GSTP2 activity, and abrogation or attenuation of genome-damaging stresses.
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Increased protein stability causes DNA methyltransferase 1 dysregulation in breast cancer. Vol. 280 (2005) 18302-18310
Agoston T. Agoston,Pedram Argani,Srinivasan Yegnasubramanian,Angelo M. De Marzo,Mohammad Ali Ansari-Lari,Jessica Hicks,Nancy E. Davidson,William G. Nelson +7 more
TL;DR: In this article, DNA methyltransferase 1 (DNMT1) expression is dysregulated in breast cancer without a concomitant increase in DNMT1 mRNA or proliferative fraction.
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Global DNA hypomethylation in intratubular germ cell neoplasia and seminoma, but not in nonseminomatous male germ cell tumors.
Georges J. Netto,Yasutomo Nakai,Masashi Nakayama,S. Jadallah,Antoun Toubaji,Norio Nonomura,Roula Albadine,Jessica Hicks,Jonathan I. Epstein,Srinivasan Yegnasubramanian,Srinivasan Yegnasubramanian,William G. Nelson,Angelo M. De Marzo +12 more
TL;DR: It is concluded that testicular germ cell tumors are derived in most cases from IGCNU cells that have undergone developmentally programmed 5mC erasure and that the degree of subsequent de novo methylation is most closely related to the differentiation state of the neoplastic cells.
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New concepts in tissue specificity for prostate cancer and benign prostatic hyperplasia
TL;DR: An evolutionary argument is presented that attempts to relate a high-fat diet, with its potential for generating oxidative DNA damage, to the species selectivity of prostate cancer and an argument based on preliminary studies indicating that chronic inflammation and the associated increase in cell turnover in the setting of increased oxidative stress may help to account for the organSelectivity of genitourinary carcinomas.
Journal ArticleDOI
Increased protein stability causes DNA methyltransferase 1 dysregulation in breast cancer
Agoston T. Agoston,Pedram Argani,Srinivasan Yegnasubramanian,Angelo M. De Marzo,Mohammad Ali Ansari-Lari,Jessica L. Hicks,Nancy E. Davidson,William G. Nelson +7 more
TL;DR: It is found thatDNMT1 protein levels were elevated in breast cancer tissues and in MCF-7 breast cancer cells relative to normal human mammary epithelial cells (HMECs) without a concomitant increase in DNMT1 mRNA or proliferative fraction.