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Articles by H An
Total Records ( 3 ) for H An
  Y. J Jang , M. S Park , S. S Park , J. H Kim , H An , S. H Park , S. J Kim , C. S Kim and Y. J. Mok
 

Background  The results of gastric cancer treatment have improved during the past 2 decades. In addition to early diagnosis, surgeon experience and subspecialty may influence long-term outcomes. This study analyzed data accumulated during the past 20 years regarding the impact of surgical subspecialty on gastric cancer prognosis.

Design  A 20-year, retrospective study.

Setting  Korea University Guro Hospital, Seoul.

Patients  A total of 2797 patients admitted between 1984 and 2003 with surgically treated, pathologically confirmed, primary gastric adenocarcinoma.

Main Outcome Measure  Long-term survival.

Results  The incidence of total gastrectomy and the number of retrieved lymph nodes increased during the study period. In curative cases, 5-year survival improved from 66.1% to 76.6%, and this survival gain was restricted to stages I, III, and IV. A Cox proportional hazards regression model showed that age, sex, tumor location, type of resection, stage, and the interaction between period of study and surgical subspecialty were independent prognostic factors.

Conclusions  This large, long-term cohort study demonstrates that the management of gastric cancer has been largely successful, with favorable trends in prognostic factors. Successful outcomes are realized more often by gastric surgical specialists. Efforts must be made to improve the treatment of patients with stage II gastric cancer because the improvements in long-term results have plateaued.

  C Wang , R Qi , N Li , Z Wang , H An , Q Zhang , Y Yu and X. Cao
 

Notch signaling plays a critical role in regulating cell proliferation, differentiation, and apoptosis. Our previous study showed that overexpression of Notch1 could inhibit human hepatocellular carcinoma (HCC) cell growth by arresting the cell cycle and inducing apoptosis. HCC cells are resistant to apoptotic induction by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), so new therapeutic approaches have been explored to sensitize HCC cells to TRAIL-induced apoptosis. We are wondering whether and how Notch1 signaling can enhance the sensitivity of HCC cells to TRAIL-induced apoptosis. In this study, we found that overexpression of ICN, the constitutive activated form of Notch1, up-regulated p53 protein expression in HCC cells by inhibiting proteasome degradation. p53 up-regulation was further observed in human primary hepatocellular carcinoma cells after activation of Notch signaling. Inhibition of the Akt/Hdm2 pathway by Notch1 signaling was responsible for the suppression of p53 proteasomal degradation, thus contributing to the Notch1 signaling-mediated up-regulation of p53 expression. Accordingly, Notch1 signaling could make HCC cells more sensitive to TRAIL-induced apoptosis, whereas Notch1 signaling lost the synergistic promotion of TRAIL-induced apoptosis in p53-silenced HepG2 HCC cells and p53-defective Hep3B HCC cells. The data suggest that enhancement of TRAIL-induced apoptosis by Notch1 signaling is dependent upon p53 up-regulation. Furthermore, Notch1 signaling could enhance DR5 expression in a p53-dependent manner. Taken together, Notch1 signaling sensitizes TRAIL-induced apoptosis in HCC cells by inhibiting Akt/Hdm2-mediated p53 degradation and up-regulating p53-dependent DR5 expression. Thus, our results suggest that activation of Notch1 signaling may be a promising approach to improve the therapeutic efficacy of TRAIL-resistant HCC.

 
 
 
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