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Sarah E. Ernst

Researcher at Johns Hopkins University School of Medicine

Publications -  11
Citations -  198

Sarah E. Ernst 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 2, co-authored 9 publications receiving 86 citations. Previous affiliations of Sarah E. Ernst include Towson University.

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Compositional differences in gastrointestinal microbiota in prostate cancer patients treated with androgen axis-targeted therapies.

TL;DR: It is speculated that oral hormonal therapies for prostate cancer may alter the GI microbiota, influence clinical responses to ATT, and/or potentially modulate the antitumor effects of future therapies including immunotherapy.
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Identifying New Small Proteins in Escherichia coli.

TL;DR: In this article, a method of small protein identification involves adding an epitope tag to the 3' end of a short open reading frame (sORF) on the chromosome, with synthesis confirmed by immunoblot assays.
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Oncogenic gene fusions in nonneoplastic precursors as evidence that bacterial infection can initiate prostate cancer.

TL;DR: In this paper, the authors investigated whether bacterial prostatitis is associated with ERG+ precancerous lesions in unique cases with active bacterial infections at the time of radical prostatectomy.
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Selenium and the 15kDa Selenoprotein Impact Colorectal Tumorigenesis by Modulating Intestinal Barrier Integrity.

TL;DR: In this paper, the authors examined the effects of Selenof on inflammatory tumorigenesis, and whether dietary selenium modified these effects, and found that the deficiency of the 15 kDa selenoprotein significantly reduced the formation of aberrant crypt foci (ACF) in a mouse model of azoxymethane (AOM)-induced colon carcinogenesis.
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Oncogenic gene fusions in non-neoplastic precursors as evidence that bacterial infection initiates prostate cancer

TL;DR: Evidence that bacterial infections initiate driver gene alterations in prostate cancer is provided, providing evidence that infection-induced ERG+ fusions are an early alteration in the carcinogenic process and PIA may serve as a direct precursor to prostate cancer.