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Chen, Peng-Chieh

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Chen

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Peng-Chieh

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Chen, Peng-Chieh

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2006 - 20082

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Author's Publications: search.filters.isAuthorOfPublication.55c37928-1bdc-49f0-b26b-ecce2f3ed395

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    Focused Ion Beam Induced Deflections of Freestanding Thin Films
    (American Institute of Physics, 2006) Kim, Young-Rok; Chen, Peng-Chieh; Aziz, Michael; Branton, Daniel; Vlassak, Joost
    Prominent deflections are shown to occur in freestanding silicon nitride thin membranes when exposed to a 50 keV gallium focused ion beam for ion doses between 1014 and 1017 ions/cm2. Atomic force microscope topographs were used to quantify elevations on the irradiated side and corresponding depressions of comparable magnitude on the back side, thus indicating that what at first appeared to be protrusions are actually the result of membrane deflections. The shape in high-stress silicon nitride is remarkably flat-topped and differs from that in low-stress silicon nitride. Ion beam induced biaxial compressive stress generation, which is a known deformation mechanism for other amorphous materials at higher ion energies, is hypothesized to be the origin of the deflection. A continuum mechanical model based on this assumption convincingly reproduces the profiles for both low-stress and high-stress membranes and provides a family of unusual shapes that can be created by deflection of freestanding thin films under beam irradiation.
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    Novel Roles for MLH3 Deficiency and TLE6-Like Amplification in DNA Mismatch Repair-Deficient Gastrointestinal Tumorigenesis and Progression
    (Public Library of Science, 2008) Chen, Peng-Chieh; Kuraguchi, Mari; Velasquez, John; Wang, Yuxun; Yang, Kan; Edwards, Robert; Gillen, Dan; Edelmann, Winfried; Kucherlapati, Raju; Lipkin, Steven M.
    DNA mismatch repair suppresses gastrointestinal tumorgenesis. Four mammalian E. coli MutL homologues heterodimerize to form three distinct complexes: MLH1/PMS2, MLH1/MLH3, and MLH1/PMS1. To understand the mechanistic contributions of MLH3 and PMS2 in gastrointestinal tumor suppression, we generated \(Mlh3^{−/−}\);\(Apc^{1638N}\) and \(Mlh3^{−/−}\);\(Pms2^{−/−}\);\(Apc^{1638N}\) (MPA) mice. Mlh3 nullizygosity significantly increased Apc frameshift mutations and tumor multiplicity. Combined Mlh3;Pms2 nullizygosity further increased Apc base-substitution mutations. The spectrum of MPA tumor mutations was distinct from that observed in \(Mlh1^{−/−}\);\(Apc^{1638N}\) mice, implicating the first potential role for MLH1/PMS1 in tumor suppression. Because Mlh3;Pms2 deficiency also increased gastrointestinal tumor progression, we used array-CGH to identify a recurrent tumor amplicon. This amplicon contained a previously uncharacterized Transducin enhancer of Split (Tle) family gene, Tle6-like. Expression of Tle6-like, or the similar human TLE6D splice isoform in colon cancer cells increased cell proliferation, colony-formation, cell migration, and xenograft tumorgenicity. Tle6-like;TLE6D directly interact with the gastrointestinal tumor suppressor RUNX3 and antagonize RUNX3 target transactivation. TLE6D is recurrently overexpressed in human colorectal cancers and TLE6D expression correlates with RUNX3 expression. Collectively, these findings provide important insights into the molecular mechanisms of individual MutL homologue tumor suppression and demonstrate an association between TLE mediated antagonism of RUNX3 and accelerated human colorectal cancer progression.