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Antitumor activity of ZD6474 in a metastatic orthotopic brain tumor model.
Kong, Doo-Sik,Kim, Mi-Hyun,Jeon, Ji-Won,Kim, Shi-Yeon,Kim, Maeng Sup,Joo, Kyeung Min,Park, Kwan,Nam, Do-Hyun D. A. Spandidos 2008 MOLECULAR MEDICINE REPORTS Vol.1 No.3
<P>The objective of this study was to examine the antitumor effect of ZD6474, an orally available inhibitor of the vascular endothelial growth factor receptor-2 (VEGFR-2) and the epidermal growth factor receptor (EGFR), on tumor growth in an orthotopic metastatic brain tumor model. In order to determine the antitumor mechanism of ZD6474 treatment, in vitro and in vivo studies were performed. Human breast carcinoma cells (MDA-MB-435) were injected using direct intracranial (IC) inoculation (5x105 cells/100 ?l) and internal carotid artery (ICA) injection (5x104 cells/100 ?l) in Balb/c-nu female mice. Daily oral treatment with ZD6474 (50 mg/kg) was initiated on day 14 after the establishment of micrometastasis. Mice (n=12 per group) were sacrificed on day 28. Western blot analysis revealed that the autophosphorylation of EGFR and Akt was increasingly decreased with ZD6474 treatment in lung and brain endothelial cells and the MDA-MB-435 cell line. MTT assay also showed that the in vitro antitumor activity of ZD6474 was dependent on EGFR tyrosine kinase inhibition at a higher dose. Daily oral treatment with ZD6474 led to marked inhibition of metastatic tumor growth in the ICA injection and the direct IC inoculation models (median size 3.5 mm3, range 1.6-13.9 mm3) as compared to the control group (median size 62.4 mm3, range 11.5-206.9 mm3). These results suggest that simultaneous inhibition of both the EGFR and VEGFR-2 signaling pathways has a valuable therapeutic effect through its inhibition of the growth of metastatic brain tumors.</P>
Kong, Kyoung Hye,Kim, Hyun Kyu,Song, Kwan Sung,Woo, Young Sik,Choi, Won Suk,Park, Hee Ra,Park, Mikyung,Kim, Mi Eun,Kim, Min-Sun,Ryu, Jeong Sim,Kim, Hyung Sik,Lee, Jaewon Taylor Francis 2010 Journal of toxicology and environmental health. Pa Vol.73 No.21
<P>Capsaicin (N-vanillyl-8-methyl-1-nonenamide) is a major pungent ingredient in hot peppers and induces apoptosis in malignant carcinoma cell lines. However, the adverse effects of capsaicin on neuronal development have not been fully explored. The aim of this study was to determine whether capsaicin affected murine-derived cerebellar multi-potent neural progenitor cells (NPC) or adult hippocampal neurogenesis in vivo. Capsaicin dose-dependently suppressed NPC proliferation, and higher concentrations were cytotoxic. Capsaicin decreased the activation of extracellular signal-regulated kinases (ERK) without markedly affecting p38 kinases. Capsaicin reduced the number of newly generated cells in the dentate gyrus of the hippocampus but did not significantly alter learning and memory performance in young adult mice. Interestingly, capsaicin decreased ERK activation in the hippocampus, suggesting that reduced ERK signaling may be involved in the capsaicin-mediated regulation of hippocampal neurogenesis.</P>
Molecular Marker Related to Fruitbody Color of Flammulina velutipes
Kong, Won-Sik,You, Chang-Hyun,Yoo, Young-Bok,Kim, Gyu-Hyun,Kim, Kwang-Ho The Korean Society of Mycology 2004 Mycobiology Vol.32 No.1
White and brown strains of Flammulina velutipes were inter-crossed. All $F_1$ showed light-brown fruitbody, suggesting that a gene for the brown fruitbody was incompletely dominant against the white one. And backcross experiment showed that more than two genes were involved in color determination. To isolate a molecular marker linked to fruitbody color, a set of primers was designed from a sequence of clones derived by a bulked segregant analysis. These markers showed a specific band which co-segregated with brown fruitbody forming strains.