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Articles by T Akimoto
Total Records ( 2 ) for T Akimoto
  K Nakamura , M Tahara , N Kiyota , R Hayashi , T Akimoto , H Fukuda , M Fujii and N. Boku
 

A Phase II study was started in Japan to evaluate the efficacy and safety of concurrent chemoradiotherapy with S-1 plus cisplatin in patients with unresectable locally advanced squamous cell carcinoma of the head and neck. This study began in July 2008, and a total of 45 patients will be accrued from 13 institutions within 2 years. The primary endpoint is the clinical complete remission rate. The secondary endpoints are local progression-free survival, overall survival, progression-free survival, time to treatment failure, proportion of patients who achieve nutritional support-free survival and adverse events.

  F Ishikawa , T Akimoto , H Yamamoto , Y Araki , T Yoshie , K Mori , H Hayashi , K Nose and M. Shibanuma
 

Mitochondrial dysfunction, in particular, interference in the respiratory chain, is often responsible for the toxicogenic effects of xenobiotics. In this study, changes in gene expression resulting from pharmacological inhibition of the respiratory chain were studied by DNA microarray analysis using cells treated with rotenone or antimycin A, which inhibit complexes I and III of the electron transport system, respectively. Forty-eight genes were either up- or down-regulated more than 3-fold. These included stress- and/or metabolic-related effector genes and several transcriptional regulators represented by CHOP-10. Further study using siRNA showed that among the four genes studied, up-regulation of three was dependent on CHOP-10. C/EBPβ, a dimerizing partner of CHOP-10, was also involved in two of the three genes including Trib3, implying that CHOP-10, heterodimerizing with C/EBPβ or another partner played a key role in the expression of a set of genes under stress. Although CHOP-10 and Trib3 were both ER-stress response genes, signal inducing Trib3 during mitochondrial stress was distinct from that during ER stress. Cytotoxicity caused by inhibition of the respiratory chain was attenuated by treatment with siRNA for CHOP-10. This study demonstrated the importance of CHOP-10 in coordinating individual gene expression in response to the mitochondrial stress.

 
 
 
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