Keijiro Araki

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A 52-year-old man suffering from a pure-type primary gastric small cell carcinoma was treated with surgery and combination chemotherapy. The small cell carcinoma, approximately 6.5 cm in diameter, was situated in the posterior wall of the antrum and there were no distant metasatses. Total gastrectomy and regional lymph node dissection was carried out.(More)
AIM To examine the paclitaxel concentrations in plasma and ascites after its intravenous administration in patients with ascites due to peritonitis carcinomatosa resulting from advanced gastric cancer. METHODS Two patients with ascites due to peritonitis carcinomatosa resulting from gastric cancer were included in this study. The paclitaxel concentrations(More)
The gastrointestinal stromal tumor cell line, GIST-T1, has a heterogenic 57-base pair deletion in exon 11 of the c-kit mutation, and the c-KIT protein in the GIST-T1 cells constitutively activated. We report that STI571 (Glivec; Novartis, Basel, Switzerland), a specific inhibitor of c-KIT, inhibits the clustering of c-KIT at the cell membrane of the GIST-T1(More)
We apply evolutionary computations to the Hop eld's neural network model of associative memory. In the model, some of the appropriate con gurations of synaptic weights give the network a function of associative memory. One of our goals is to obtain the distribution of these con gurations in the synaptic weight space. In other words, our aim is to learn a(More)
We analyzed the clinicopathologic variables and postoperative outcomes in patients with extrahepatic adenosquamous carcinoma to identify important factors for predicting postresection prognosis. Thirty-six patients in Japan who underwent surgical resection for adenosquamous carcinoma of the extrahepatic biliary tract, with curative intent by the end of(More)
AIM To estimate whether STI571 inhibits the expression of vascular endothelial growth factor (VEGF) in the gastrointestinal stromal tumor (GIST) cells. METHODS We used GIST cell line, GIST-T1. It has a heterogenic 57-bp deletion in exon 11 to produce a mutated c-KIT, which results in constitutive activation of c-KIT. Cells were treated with/without STI571(More)