Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
 
Articles by S Abe
Total Records ( 3 ) for S Abe
  Y Kimura , F. T Nishimura , S Abe , T Fukunaga , H Tanii and K. Saijoh
 

Aims: To assess the effect of the –360G/A polymorphism in the promoter region of the human aldehyde dehydrogenase-2 (ALDH2) gene on its transcription, basal and acetaldehyde/ethanol-induced gene expression was examined by in vivo and in vitro experiments. Methods: Human peripheral blood leukocytes were collected before and after alcohol ingestion (0.4 g/kg body weight) in 21 healthy young Japanese volunteers with a deficient phenotype of ALDH2 (487Glu/Lys), and the levels of ALDH2 mRNA were quantified by real-time RT-PCR. The transcriptional activity of the ALDH2 promoter was investigated by a reporter assay using HepG2 cells in the presence or absence of acetaldehyde/ethanol. Results: The basal level of ALDH2 mRNA was significantly higher in –360A heterozygous subjects than in –360G homozygous subjects. In all subjects, regardless of the genotype, ALDH2 mRNA increased following ethanol ingestion. The promoter activity of a reporter plasmid for –360G was significantly lower than that of a reporter plasmid for –360A. Exposure to acetaldehyde induced a significant increase in the transcriptional activity of the –360G reporter, but not the –360A reporter. Conclusions: In vivo and in vitro experiments showed that the –360G allele has lower basal transcriptional activity than the –360A allele, whereas acetaldehyde/ethanol-induced gene expression, in general, seems to be more enhanced in individuals homozygous for the –360G allele than in those with the –360A allele. Thus, the promoter polymorphism may be involved in individual differences in acetaldehyde elimination.

  O Itano , K Yang , K Fan , N Kurihara , H Shinozaki , S Abe , B Jin , C Gravaghi , W Edelmann , L Augenlicht , L Kopelovich , R Kucherlapati , S Lamprecht and M. Lipkin
 

We have previously reported that sulindac, a non-steroidal anti-inflammatory drug, inhibited tumor formation in the small intestine but increased tumors in the colon of ApcMin/+ mice, a model of human familial adenomatous polyposis. To further explore intestinal regional responses, we studied effects of sulindac on additional gene-targeted mouse models of human intestinal tumorigenesis; these were (i) Apc1638N/+ mouse (chain termination mutation in exon 15 of the Apc gene); (ii) Mlh1+/– mouse (DNA mismatch repair deficiency, a mouse model of human hereditary non-polyposis colorectal cancer) and (iii) double-heterozygous Mlh1+/–Apc1638N/+ mutant mouse. Mice were fed AIN-76A control diet with or without 0.02% sulindac for 6 months. Intestinal regional tumor incidence, multiplicity, volume and degree of inflammation were used as end points. The results showed the following: (i) sulindac inhibited tumor development in the small intestine of Apc1638N/+ mice; (ii) in contrast, sulindac increased tumors in the small intestine of Mlh1 mutant mice, a neoplastic effect which persisted in heterozygous compound Mlh1+/–Apc1638N/+ mutant mice; (iii) sulindac increased tumors in the cecum of all mice regardless of genetic background; (iv) sulindac decreased inflammation in the small intestine of Apc1638N/+ mice, but it increased inflammation in the small intestine of Mlh1+/ mice and Mlh1+/–Apc1638N/+ mice and (v) sulindac enhanced inflammation in the cecum of all mutant mice. Findings indicate that the effects of sulindac in the intestine of these mutant mouse models are probably related to genetic background and appear to be associated with its inflammatory-inducing response.

  S Abe , Y Tsuji , T Tsushima , T Kogawa , M Abe , Y Onodera , T Mizushima , T Kukitsu , T Sumiyoshi , N Yoshizaki , T Ishii and H. Kondo
  Objective

Although combination chemotherapy with 3 weeks of S-1 and cisplatin is effective for advanced gastric cancer, the toxicities of S-1 which mostly occur during the third week of administration are a major problem. To achieve fewer adverse effects with S-1 and higher dose intensity of cisplatin, we performed combination chemotherapy with 2 weeks of S-1 and cisplatin as first line. The aim of this retrospective study was to analyse the efficacy and feasibility of this regimen.

Methods

S-1 (40–60 mg depending on patient's body surface area) was given orally twice daily for 2 consecutive weeks, and 70 mg/m2 cisplatin was given intravenously on day 8, followed by a 2-week rest period.

Results

Forty-eight patients received a total of 184 courses of chemotherapy. Overall response rate was 40.6% and median survival time was 411 days. Dose intensities were 257.6 mg/m2/week for S-1 and 16.4 mg/m2/week for cisplatin. The incidences of grade 3/4 haematological toxicities were leucopenia (19%), neutropenia (29%) and anaemia (17%), and those of grade 3 non-haematological toxicities were anorexia (31%) and nausea (21%). The rate of treatment discontinuation owing to toxicity was 10%.

Conclusions

This regimen may be effective as an alternative therapy to 3 weeks of S-1 and cisplatin to reduce the toxicity of chemotherapy for advanced gastric cancer.

 
 
 
Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility