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- W3023883313 abstract "Standard treatments have little impact against pancreatic cancer and research is focusing on agents targeting molecular pathways involved in tumor growth and angiogenesis, such as ZD6474, an orally available inhibitor of VEGFR-2, and EGFR tyrosine kinase activity. This study investigated potential interactions between ZD6474, gemcitabine and ionizing radiation in human pancreatic cancer cells, and analyzed potential underlying cellular and genetic mechanisms. MIA PaCa-2, PANC-1 and Capan-1 cells and MIA PaCa-2 tumor xenografts were treated with ZD6474, ionizing radiation and gemcitabine alone or in combination. Effects on phosphorylation of EGFR and Akt were investigated by ELISA. Apoptosis was studied by fluorescence microscopy and quantitative PCR was used to study target gene expression profiles. In vitro, ZD6474 dose-dependently inhibited pancreatic tumor cell growth, inducing apoptosis and synergistically enhancing the cytotoxic activity of gemcitabine and ionizing radiation. Moreover, ZD6474 inhibited phosphorylation of EGFR and Akt, and increased tumor cell apoptosis. PCR analysis showed that ZD6474 increased the gene expression ratio between the gemcitabine activating enzyme deoxycytidine kinase and the gemcitabine target ribonucleotide reductase. In vivo, ZD6474 demonstrated significant antitumor activity alone and in combination with radiotherapy and gemcitabine, and the combination of all three modalities enhanced MIA PaCA-1 tumor growth inhibition compared with gemcitabine alone. ZD6474 decreases EGFR and Akt phosphorylation, increases apoptosis and gene expression in human pancreatic tumor cells, and acts synergistically with gemcitabine and radiotherapy to inhibit tumor cell growth. These data provide a scientific rationale to investigate this combination in pancreatic cancer in the clinic." @default.
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- W3023883313 date "2006-11-01" @default.
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- W3023883313 title "2162" @default.
- W3023883313 doi "https://doi.org/10.1016/j.ijrobp.2006.07.567" @default.
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