林 秀樹

Background. Perioperative steroid therapy has been shown to be safe and effective in inhibiting the production of inflammatory mediators and reducing postoperative hospital morbidity. However, there is limited information to show the effect of steroid therapy on long-term survival. In this study we evaluated the effect of perioperative steroid therapy on long-term survival of patients with thoracic esophageal cancer. Methods. Between 1993 and 2000, 141 consecutive patients with primary thoracic esophageal cancer underwent radical esophagectomy. A total of 78 patients who underwent surgery between 1997 and 2000 received perioperative steroid therapy. Sixty-three patients who underwent surgery between 1993 and 1996 were analyzed as the control group. In the steroid group, 250mg methylprednisolone was administered intravenously just before surgery followed by 125mg on postoperative days 1 and 2. The postoperative course and overall cause-specific survival rates were compared between the groups. Results. The postoperative hospital morbidity rate was significantly lower in the steroid group than in the control group. Although overall survival of the steroid group was better than the control group, cause-specific survival of both groups was similar. Multivariate analysis suggested that the depth of tumor and postoperative hospital morbidity were significant independent prognostic factors however, steroid therapy was not statistically significant after adjusting for pathological variables. Conclusions. Perioperative steroid therapy may improve the postoperative course but does not improve the longterm survival of patients with thoracic esophageal cancer. © Japan Esophageal Society and Springer-Verlag 2004.

BACKGROUND, The primary objective of this study was to clarify the significance of p21(WAF1/CIP1)(p21) gene expression in the tumorgenicity of hepatitis B virus (HBV) and hepatitis C virus (HCV) infected human hepatocelluar carcinoma (HCC). METHODS. The authors performed Northern blot hybridization to compare the p21 messenger (m) RNA expression levels among 16 HCC cases. They detected tissue HBVx mRNA (Northern blot) and plus- and minus-strand HCV RNA (reverse transcription-polymerase chain reaction) in liver tissues. They also measured alanine transaminase (ALT) levels and indocyanine green retention rate at 15 minutes (ICG-R15). RESULTS. The p21 transcripts of tumor (T) tissues could be identified with lower intensity than nontumor (N) tissues in all 4 HBVx mRNA(+) cases, 8 of 10 HCV RNA(+) cases, and 1 of 3 B(-), C(-) cases (1 case was positive for both viruses). p21 mRNA expression levels of N tissues were significantly higher in HCV RNA(+) cases than in HBVx mRNA(+) cases. p21 mRNA expression levels of N tissues were significantly correlated with serum ALT levels. CONCLUSIONS. In HCV hepatitis, p21 mRNA expression is up-regulated to control cell cycle under regeneration stress. Once the liver develops HCC, the p21 mRNA expression decreases to prominently low levels. The up-regulated p21 expression may play a role as a guard to prevent hepatocytes from tumorgenicity in HCV hepatitis. Cancer 2001;91:2096-103. (C) 2001 American Cancer Society.