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Articles by H. K Yang
Total Records ( 3 ) for H. K Yang
  S. H Hwang , D. J Park , Y. S Jee , M. C Kim , H. H Kim , H. J Lee , H. K Yang and K. U. Lee
 

Objective  To analyze 3-year actual disease-free survival after laparoscopy-assisted gastrectomy for gastric cancer on the assumption that 3-year disease-free survival may represent 5-year overall survival.

Design  Retrospective analysis.

Setting  Department of surgery of a university hospital.

Patients  A total of 197 patients who underwent laparoscopy-assisted gastrectomy for gastric cancer from May 1998 to September 2007 and who were followed up for more than 3 years.

Main Outcome Measures  Feasibility and long-term survival rate with survival analysis by the Kaplan-Meier method.

Results  Subtotal and total gastrectomies were performed in 178 and 19 patients, respectively. The scope of the lymph node dissections were D1 + β (n = 152) and D2 (n = 45). There were 153, 28, 8, 6, 1, and 1 patients in stages Ia, Ib, II, IIIa, IIIb, and IV, respectively. The median follow-up was 45 months (range, 1-113 months), and there were 7 recurrences. Multivariate analysis of disease-specific survival showed that depth of invasion and lymph node metastasis influenced the prognosis independently. The actual 3-year disease-free survival rate for all patients was 96.9%. The 173 patients with early gastric cancer and 24 with advanced gastric cancer showed 98.8% and 79.1% actual 3-year disease-free survival rates, respectively.

Conclusions  Laparoscopy-assisted gastrectomy is acceptable oncologically in early gastric cancer if 3-year disease-free survival represents 5-year overall survival. Laparoscopy-assisted gastrectomy may also play an important role in the treatment of advanced gastric cancer.

  J. S Kang , S Y.Bae , H R.Kim , Y. S Kim , D J.Kim , B. J Cho , H. K Yang , Y. I Hwang , K J.Kim , H. S Park , D H.Hwang , D J.Cho and W. J. Lee
 

Cancer cells metastasize to the other site after escaping from the immune system and CD70, CD44 and vascular endothelial growth factor (VEGF) play important roles in this process. It is recently reported that interleukin (IL)-18 is closely related with the pathogenesis of skin tumor. Therefore, we investigated the role of endogenous IL-18 from stomach cancer on the immune escape mechanism and metastasis via the regulation of CD70, CD44 and VEGF expression. IL-18 and IL-18R expressions were not only investigated on tumor tissues (n = 10), and sera (n = 20) from stomach cancer patients, but also on human stomach cancer cell lines. IL-18 and IL-18R expressions were found on stomach cancer cell lines and tumor tissues. In addition, IL-18 levels were elevated in sera from cancer patients (P < 0.05), compared with sera from normal individuals. Changes in CD70, CD44 and VEGF expression by flow cytometry, immunoblotting and enzyme-linked immunosorbent assay and immune susceptibility by 51Cr-release assay were investigated, after silencing or neutralization of endogenous IL-18. CD70 expression was increased and it increases immune susceptibility of cancer cells. In contrast, CD44 and VEGF expression was decreased and it suppresses neovascularization and the metastasis of stomach cancer. After inoculation of IL-18 small interfering RNA (siRNA)-transfected stomach cancer cells into Balb/C (nu/nu) mice, regression of tumor mass was determined by measuring of tumor size. And the number and location of metastatic lesions were investigated by hematoxylin and eosin staining. The regression of tumor mass and the suppression of metastasis were observed in the mice, which are injected with IL-18 siRNA-transfected cell lines. Our data suggest that endogenous IL-18 might facilitate stomach cancer cell immune escape by suppressing CD70 and increasing metastatic ability by upregulating CD44 and VEGF.

 
 
 
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