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Articles by T Shimazu
Total Records ( 3 ) for T Shimazu
  M Inoue , N Kurahashi , M Iwasaki , T Shimazu , Y Tanaka , M Mizokami , S Tsugane and for the Japan Public Health Center Based Prospective Study Group

In spite of their anticarcinogenic potential, the effect of coffee and green tea consumption on the risk of liver cancer has not been clarified prospectively in consideration of hepatitis C (HCV) and B virus (HBV) infection. We examined whether coffee and green tea consumption was associated with a reduced risk of liver cancer by hepatitis virus infection status in the Japan Public Health Center-Based Prospective Study Cohort II. A total of 18,815 subjects ages 40 to 69 years participating in a questionnaire and health checkup survey in 1993 to 1994 were followed for the incidence of liver cancer through 2006. A total of 110 cases of liver cancer were newly documented. Hazard ratios for coffee and green tea consumption categories were calculated with a Cox proportional hazards model. Compared with almost never drinkers, increased coffee consumption was associated with a reduced risk of liver cancer in all subjects (hazard ratio for <1, 1-2, and ≥3 cups/d; Ptrend = 0.67, 0.49, 0.54, and 0.025). A similar risk tendency was observed in those with either or both HCV and HBV infection. In contrast, no association was observed between green tea consumption and the risk of liver cancer in all subjects. Our results suggest that coffee consumption may reduce the risk of liver cancer regardless of HCV and HBV infection status, whereas green tea may not reduce this risk.(Cancer Epidemiol Biomarkers Prev 2009;18(6):1746–53)

  S Sasazuki , M Inoue , N Sawada , M Iwasaki , T Shimazu , T Yamaji , S Tsugane and for the Japan Public Health Center Based Prospective Study Group

Gastric carcinogenesis may be under the combined influence of factors related to the host, Helicobacter pylori bacterial virulence and the environment. One possible host-related factor is the inflammatory or immune response. To clarify this point, we investigated the association between plasma levels of C-reactive protein (CRP) and serum amyloid A (SAA) and the subsequent risk of gastric cancer in a population-based nested case–control study. Subjects were observed from 1990 to 2004. Among 36 745 subjects who answered the baseline questionnaire and provided blood samples, 494 gastric cancer cases were identified and matched to 494 controls for our analysis. The overall distribution of CRP and SAA was not apparently associated with the development of gastric cancer. However, a statistically significant increased risk was observed when subjects were categorized dichotomously. The adjusted odds ratio (OR) for the development of gastric cancer for the CRP-positive group (CRP > 0.18 mg/dl) compared with the CRP-negative group was 1.90 [95% confidence interval (CI): 1.19–3.02, P = 0.007]. The OR for the SAA-positive group (SAA > 8 µg/ml) compared with the SAA-negative group was 1.93 (95% CI: 1.22–3.07, P = 0.005). In conclusion, our results suggest that those who react strongly to inflammation or who have a high host immune response, as reflected by extremely elevated plasma levels of CRP and SAA, are at a high risk to develop gastric cancer.

  H Takeshima , S Yamashita , T Shimazu , T Niwa and T. Ushijima

Instructive mechanisms are present for induction of DNA methylation, as shown by methylation of specific CpG islands (CGIs) by specific inducers and in specific cancers. However, instructive factors involved are poorly understood, except for involvement of low transcription and trimethylation of histone H3 lysine 27 (H3K27me3). Here, we used methylated DNA immunoprecipitation (MeDIP) combined with a CGI oligonucleotide microarray analysis, and identified 5510 and 521 genes with promoter CGIs resistant and susceptible, respectively, to DNA methylation in prostate cancer cell lines. Expression analysis revealed that the susceptible genes had low transcription in a normal prostatic epithelial cell line. Chromatin immunoprecipitation with microarray hybridization (CHiP-chip) analysis of RNA polymerase II (Pol II) and histone modifications showed that, even among the genes with low transcription, the presence of Pol II was associated with marked resistance to DNA methylation (OR = 0.22; 95% CI = 0.12–0.38), and H3K27me3 was associated with increased susceptibility (OR = 11.20; 95% CI = 7.14–17.55). The same was true in normal human mammary epithelial cells for 5430 and 733 genes resistant and susceptible, respectively, to DNA methylation in breast cancer cell lines. These results showed that the presence of Pol II, active or stalled, and H3K27me3 can predict the epigenetic fate of promoter CGIs independently of transcription levels.

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