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Catherine Pettit

Researcher at Johns Hopkins University

Publications -  5
Citations -  882

Catherine Pettit is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Estrogen receptor & Estrogen receptor alpha. The author has an hindex of 5, co-authored 5 publications receiving 824 citations.

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Anticancer activities of novel chalcone and bis-chalcone derivatives

TL;DR: Novel chalcones and bis-chalcones containing boronic acid moieties inhibited the growth of the human breast cancer cell lines at low micromolar to nanomolar concentrations and exhibited more potent inhibition of colon cancer cells expressing wild-type p53 than of an isogenic cell line that was p53-null.
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Design, synthesis, and evaluation of novel boronic-chalcone derivatives as antitumor agents.

TL;DR: In this paper, a series of boronic-chalcone derivatives were synthesized and tested for antitumor activity against human breast cancer cell lines, and the results showed that the chalcone derivatives are more toxic to breast cancer cells compared to normal breast cells than other known chalcones.
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A Novel Histone Deacetylase Inhibitor, Scriptaid, Enhances Expression of Functional Estrogen Receptor α (ER) in ER negative human breast cancer cells in combination with 5-aza 2′-deoxycytidine

TL;DR: The results indicate that the novel HDAC inhibitor, Scriptaid, inhibits tumor growth in vitro and in vivo and, in conjunction with AZA, acts to re-express functional ER.
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Protein Phosphatase 2A Regulates Estrogen Receptor α (ER) Expression through Modulation of ER mRNA Stability

TL;DR: Investigation of the effect of PP2A on regulation of ER expression in the human breast cancer cell line MCF-7 suggested a novel pathway controlling ER expression resulting from the activation ofPP2A, potentially providing a novel therapeutic target.
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Epigenetic regulation of protein phosphatase 2A (PP2A), lymphotactin (XCL1) and estrogen receptor alpha (ER) expression in human breast cancer cells

TL;DR: Through the use of pharmacologic inhibitors, 5-aza 2’deoxycytidine (AZA) and Trichostatin A (TSA), it is shown that alterations in both of these mechanisms results in synergistic re-expression of ER mRNA and functional protein.