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Michael A. Gordon

Researcher at Anschutz Medical Campus

Publications -  12
Citations -  882

Michael A. Gordon is an academic researcher from Anschutz Medical Campus. The author has contributed to research in topics: Triple-negative breast cancer & Enzalutamide. The author has an hindex of 10, co-authored 12 publications receiving 664 citations. Previous affiliations of Michael A. Gordon include University of Colorado Denver.

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A TDO2-AhR signaling axis facilitates anoikis resistance and metastasis in triple-negative breast cancer.

TL;DR: An NF-κB-regulated signaling axis that promotes anoikis resistance is defined, functional connections with inflammatory modulation by the kynurenine pathway are suggested, and TDO2 is highlighted as an attractive target for treatment of this aggressive breast cancer subtype.
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Multiple molecular subtypes of triple-negative breast cancer critically rely on androgen receptor and respond to enzalutamide in vivo.

TL;DR: It is indicated that non-LAR subtypes of TNBC are AR dependent and, moreover, that enzalutamide is a promising targeted therapy for multiple molecular sub types of AR+ TNBC.
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Cooperative Dynamics of AR and ER Activity in Breast Cancer

TL;DR: Preclinical evidence is provided that anti-androgens that inhibit AR nuclear localization affect both AR and ER, and are effective in combination with current breast cancer therapies, and that enzalutamide may be an effective therapeutic in ER+/AR+ breast cancers.
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Androgen Receptor Biology in Triple Negative Breast Cancer: a Case for Classification as AR+ or Quadruple Negative Disease

TL;DR: It is proposed that TNBC be further sub-classified as either AR+ TNBC or quadruple negative breast cancer since targeting AR may represent a viable therapeutic option for a subset of TNBC.
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The long non-coding RNA MALAT1 promotes ovarian cancer progression by regulating RBFOX2-mediated alternative splicing.

TL;DR: The lncRNA MALAT1 facilitates a pro‐metastatic phenotype in ovarian cancer by promoting alternative RNA processing and differential expression of anti‐apoptosis and epithelial to mesenchymal transition (EMT)‐related genes.