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Yuhong Lu
Researcher at Yale University
Publications - 13
Citations - 1717
Yuhong Lu is an academic researcher from Yale University. The author has contributed to research in topics: DNA repair & Cancer cell. The author has an hindex of 9, co-authored 13 publications receiving 1604 citations. Previous affiliations of Yuhong Lu include McGill University.
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Journal ArticleDOI
Insulin-like growth factor-I receptor signaling and resistance to trastuzumab (Herceptin)
TL;DR: In breast cancer cell models that overexpress HER2/neu, an increased level of IGF-IR signaling appears to interfere with the action of trastuzumab, and strategies that target IGF- IR signaling may prevent or delay development of resistance to trastzumab.
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Molecular mechanisms underlying IGF-I-induced attenuation of the growth-inhibitory activity of trastuzumab (Herceptin) on SKBR3 breast cancer cells
TL;DR: The results provide an example of resistance to an antineoplastic therapy that targets one tyrosine kinase receptor by increased signal transduction through an alternative pathway in a complex regulatory network.
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Inhibition of poly(ADP-ribose) polymerase down-regulates BRCA1 and RAD51 in a pathway mediated by E2F4 and p130
Denise C. Hegan,Yuhong Lu,Gregory C. Stachelek,Meredith E. Crosby,Ranjit S. Bindra,Peter M. Glazer +5 more
TL;DR: It is shown that PARP inhibition to block BER is toxic to hypoxic cancer cells, in which homology-dependent repair (HDR) is known to be down-regulated, and direct measurement of HDR using a GFP-based assay demonstrates reduced HDR in cells treated with PARP inhibitors.
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Hypoxia-Induced Epigenetic Regulation and Silencing of the BRCA1 Promoter
TL;DR: It is shown that hypoxia also drives epigenetic modification of the BRCA1 promoter, with decreased H3K4 methylation as a key repressive modification produced by the lysine-specific histone demethylase LSD1.
Journal Article
Co-targeting HER2/ErbB2 and insulin-like growth factor-1 receptors causes synergistic inhibition of growth in HER2-overexpressing breast cancer cells.
TL;DR: Observations support the concept that simultaneously co-targeting tyrosine kinase receptors may be therapeutically useful, and provide a specific rationale for combining IGF-1R and HER2/erbB2 targeting strategies in anti-neoplastic approaches.