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Helen Cheng

Researcher at University of British Columbia

Publications -  8
Citations -  680

Helen Cheng is an academic researcher from University of British Columbia. The author has contributed to research in topics: Androgen receptor & Prostate cancer. The author has an hindex of 7, co-authored 8 publications receiving 652 citations.

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Characterization of two cis-acting DNA elements involved in the androgen regulation of the probasin gene.

TL;DR: The preferential androgen regulation of the PB gene involves the participation of two different cis-acting DNA elements that bind AR, which is more effectively induced by androgens than by glucocorticoids or progestins.
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Short Hairpin RNA Knockdown of the Androgen Receptor Attenuates Ligand-Independent Activation and Delays Tumor Progression

TL;DR: By inducibly suppressing AR expression in vivo, there is an extensive delay in progression to androgen independence as well as a dramatic inhibition of tumor growth and decrease in serum PSA, which exceeds that seen with castration alone.
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The expression of glucocorticoid receptor is negatively regulated by active androgen receptor signaling in prostate tumors.

TL;DR: GR expression is negatively regulated by AR signaling and may serve as a marker for AR signaling in prostate tumors, and is inversely correlated with AR and PSA expressions.
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Cortisol alters gene expression during involution of the rat ventral prostate.

TL;DR: The ability of high doses of cortisol to retard the involution process in the rat ventral prostate was related to alterations in the pattern of gene expression, which modified the expression of genes associated with prostatic cell death.
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TAF1 differentially enhances androgen receptor transcriptional activity via its N-terminal kinase and ubiquitin-activating and -conjugating domains.

TL;DR: Increased TAF1 expression is associated with progression of human prostate cancers to the lethal castration-resistant state and its overexpression could be part of a compensatory mechanism adapted by cancer cells to overcome reduced levels of circulating androgens.