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Kenneth P. Nephew

Researcher at Indiana University

Publications -  284
Citations -  17018

Kenneth P. Nephew is an academic researcher from Indiana University. The author has contributed to research in topics: Ovarian cancer & DNA methylation. The author has an hindex of 66, co-authored 267 publications receiving 15106 citations. Previous affiliations of Kenneth P. Nephew include University of Tennessee Health Science Center & Indiana University – Purdue University Indianapolis.

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Dominant-negative histone H3 lysine 27 mutant derepresses silenced tumor suppressor genes and reverses the drug-resistant phenotype in cancer cells.

TL;DR: The results show that overexpression of mutant H3-K27 in mammalian cells represents a novel tool for studying epigenetic mechanisms and the Histone Code Hypothesis in human cancer, and show the significance of H2K27 methylation as a promising target for epigenetic-based cancer therapies.
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Therapeutic targeting using tumor specific peptides inhibits long non-coding RNA HOTAIR activity in ovarian and breast cancer.

TL;DR: A peptide nucleic acids (PNA)-based approach to block the ability of HOTAIR to interact with EZH2 and subsequently inhibit HOTAIS activity and resensitize resistant ovarian tumors to platinum suggests a novel cancer therapeutic approach.
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Inhibition of MCL-1 enhances Lapatinib toxicity and overcomes lapatinib resistance via BAK-dependent autophagy

TL;DR: The data demonstrate that Obatoclax mediated inhibition of MCL-1 rapidly enhances Lapatinib toxicity in tumor cells via a toxic form of autophagy and via AIF release from the mitochondrion.
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Epigenetic therapies for chemoresensitization of epithelial ovarian cancer

TL;DR: Based on promising preclinical studies, DNA methylation inhibitors in combination with existing chemotherapeutic agents have the potential for overcoming acquired drug resistance, laying the foundation for this specific class of epigenetic drug in ovarian cancer clinical trials.
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Strain differences in vaginal responses to the xenoestrogen bisphenol A.

TL;DR: F344 and S-D rats exhibit differences in sensitivity to BPA at the level of cell proliferation in the vaginal epithelium, but metabolic clearance of BPA and the early events that lead to the proliferative response, receptor-ligand interaction and induction of immediate early genes, show no strain differences.