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Articles by H. H Kim
Total Records ( 5 ) for H. H Kim
  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.

  I. L Romero , I. O Gordon , S Jagadeeswaran , K. L Mui , W. S Lee , D. M Dinulescu , T. N Krausz , H. H Kim , M. L Gilliam and E. Lengyel
 

Although epidemiologic evidence for the ability of combined oral contraception (OC) to reduce the risk of ovarian cancer (OvCa) is convincing, the biological mechanisms underlying this effect are largely unknown. We conducted the present study to determine if OC also influences ovarian carcinogenesis in a genetic mouse model and, if so, to investigate the mechanism underlying the protective effect. LSL-K-rasG12D/+PtenloxP/loxP mice were treated with ethinyl estradiol plus norethindrone, contraceptive hormones commonly used in combined OC, or norethindrone alone, or a gonadotropin-releasing hormone agonist. The combined OC had a 29% reduction in mean total tumor weight compared with placebo (epithelial tumor weight, –80%). Norethindrone alone reduced mean total tumor weight by 42% (epithelial tumor weight, –46%), and the gonadotropin-releasing hormone agonist increased mean total tumor weight by 71% (epithelial tumor weight, +150%). Large variations in tumor size affected the P values for these changes, which were not statistically significant. Nonetheless, the OC reductions are consistent with the epidemiologic data indicating a protective effect of OC. Matrix metalloproteinase-2 activity was decreased in association with OC, indicating that OC may affect ovarian carcinogenesis by decreasing proteolytic activity, an important early event in the pathogenesis of OvCa. In contrast, OC increased invasion in a K-ras/Pten OvCa cell line established from the mouse tumors, suggesting that OC hormones, particularly estrogen, may have a detrimental effect after the disease process is under way. Our study results support further investigation of OC effects and mechanisms for OvCa prevention.

  H. H Kim , Y Kuwano , S Srikantan , E. K Lee , J. L Martindale and M. Gorospe
 

RNA-binding proteins (RBPs) and microRNAs (miRNAs) are potent post-transcriptional regulators of gene expression. Here, we show that the RBP HuR reduced c-Myc expression by associating with the c-Myc 3' untranslated region (UTR) next to a miRNA let-7-binding site. Lowering HuR or let-7 levels relieved the translational repression of c-Myc. Unexpectedly, HuR and let-7 repressed c-Myc through an interdependent mechanism, as let-7 required HuR to reduce c-Myc expression and HuR required let-7 to inhibit c-Myc expression. Our findings suggest a regulatory paradigm wherein HuR inhibits c-Myc expression by recruiting let-7-loaded RISC (RNA miRNA-induced silencing complex) to the c-Myc 3'UTR.

  J. H Ku , K. C Moon , C Kwak , H. H Kim and S. E. Lee
  Objective

The aim of this study was to compare type 1 and type 2 papillary renal cell carcinoma (RCC) for validating this subclassification as a prognostic factor.

Methods

A total of 70 patients with chromophobe RCC were included in the analysis. Patients with papillary RCC were categorized into type 1 (n = 33) and type 2 (n = 37).

Results

The median progression-free survival was 31.0 months for the type 1 group and 12.0 months for the type 2 group (P = 0.001). The median cancer-specific survival was 41.1 months for the type 1 group and 24.0 months for the type 2 group (P = 0.097). Multivariate Cox proportional hazards model for patients with papillary RCC showed that no variables including histologic subtyping were independent predictors of progression-free and cancer-specific survival.

Conclusions

In the present study, the type of papillary RCC does not reach independent prognostic significance.

 
 
 
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