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Articles by W. J. Lee
Total Records ( 3 ) for W. J. Lee
  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.

  S. A. Lee , W. J. Lee , E. H. Kim , J. H. Yu , C. H. Jung , E. H. Koh , M.-S. Kim , J.-Y. Park and K.-U. Lee
  Aims: To investigate the rate of progression to insulin deficiency in Korean patients with Type 2 diabetes mellitus positive for anti-GAD antibody (GADA) and to determine the factors related to progression to insulin deficiency. Methods: We retrospectively analysed data on 87 GADA-positive and 87 age- and sex-matched GADA-negative patients with Type 2 diabetes. GADA-positive patients were further subclassified into high-titre (≥ 250 WHO units/ml) (n = 24) and low-titre (< 250 WHO units/ml) (n = 63) subgroups. Cox proportional hazard analysis was used to identify factors associated with progression to insulin deficiency. Results: Over a period of 6 years, two of 87 (2.3%) GADA-negative and 37 of 87 (42.5%) GADA-positive patients had progressed to insulin deficiency. The rate of progression to insulin deficiency was higher in the high-titre than in the low-titre subgroup (75.0 vs. 30.2%). Multivariate analysis in GADA-positive patients showed that high-titre GADA and low BMI at diagnosis were independent factors significantly related to progression to insulin deficiency. Conclusions: The presence of GADA predicted the progression to insulin deficiency in Korean patients with Type 2 diabetes. In GADA-positive patients, high-titre GADA and low BMI were associated with this progression.
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