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Margaret T. Willard

Researcher at Emory University

Publications -  10
Citations -  1940

Margaret T. Willard is an academic researcher from Emory University. The author has contributed to research in topics: Hypoxia-inducible factors & Angiogenesis. The author has an hindex of 10, co-authored 10 publications receiving 1835 citations.

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2ME2 inhibits tumor growth and angiogenesis by disrupting microtubules and dysregulating HIF.

TL;DR: These data establish 2ME2 as a small molecule inhibitor of HIF-1 and provide a mechanistic link between the disruption of the MT cytoskeleton and inhibition of angiogenesis.
Journal Article

Geldanamycin Induces Degradation of Hypoxia-inducible Factor 1α Protein via the Proteosome Pathway in Prostate Cancer Cells

TL;DR: It is shown that treatment of prostate cancer PC-3 and LNCaP cells with the benzoquinone ansamycin geldanamycin, an Hsp90-specific inhibitor, induced degradation of HIF-1alpha protein in a dose- and time-dependent manner under both normoxia and hypoxia.
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CXCR4/CXCL12 axis promotes VEGF-mediated tumor angiogenesis through Akt signaling pathway.

TL;DR: This study demonstrates that the CXCR4/CXCL12 signaling axis can induce angiogenesis and progression of tumors by increasing expression of VEGF through the activation of PI3K/Akt pathway.
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Human Tumor Antigens Tn and Sialyl Tn Arise from Mutations in Cosmc

TL;DR: Diverse neoplastic lesions, including colon cancer and melanoma-derived cells lines, expressed both Tn and STn antigen due to loss-of-function mutations in Cosmc, the first example of somatic mutations in multiple types of cancers that cause global alterations in cell surface carbohydrate antigen expression.
Journal Article

Androgens Stimulate Hypoxia-inducible Factor 1 Activation via Autocrine Loop of Tyrosine Kinase Receptor/Phosphatidylinositol 3′-Kinase/Protein Kinase B in Prostate Cancer Cells

TL;DR: Androgens activate HIF-1, driving VEGF expression in androgen-sensitive LNCaP cells, and this regulation is mediated through an autocrine loop involving EGF/phosphatidylinositol 3'-kinase/protein kinase B, which in turn activate Hif-1alpha and H IF-1-regulated gene expression.