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Background/Aims: The aim of this study was to study the role of Helicobacter pylori infection and cagA expression in gastric carcinogenesis. Methods: One hundred forty six patients were divided into three groups. Case group included 50 patients with gastric adenocarcinoma. Control group 1 included 38 patients with nongastric cancer, and control group 2 included 58 patients with nonulcer dyspepsia Biopsy specimens were evaluated to detect the presence of Helicobacter pylori by histology, rapid urease test and reverse transcription-polymerase chain reaction (RT-PCR) using primers specific for 16S rRNA and cagA mRNA of Helicobacter pylori. Results: The expression rates of 16S rRNA and cagA mRNA of Helicobacter pylori in patients with gastric carcinoma were 74% and 51%, respectively. Although 90% of patients with gastric carcinoma had Helicobacter pylori infection, the significant association between Helicobacter pylori infection and gastric carcinoma was not observed. There was no significant association between cagA expression and gastric carcinoma. Conclusions: Helico bacter pylori infection and cagA expression were not associated with the risk of gastric carcinoma (Kor J Gastroenterol 1999;33:321 - 330)
Purpose: Hepatocellular carcinoma(HCC) is the most common form of primary hepatic carcinoma and is considered to be a highly malignant tumor with poor prognosis. We evaluated the efficacy and toxicities of AP(doxorubicin, cisplatin) comnination chemotherapy in hepatocellular carcinoma. Materials and Methods: Between October 1989 and February 1991, 21 previously untreated patients with advanced hepatocellular carcinoma were entered and treated with AP combination chemotherapy(adriamycin 60 mg/m2, D1 and cisplatin 60 mg/m, D1, repeated every 3 weeks). Results: Among 14 evaluable patients, there was no complete response and 5 patients (36%; 95% C.I=10-62%) achieved partial response. The median survival time of all 21 patients was 17 weeks, and 63 weeks in responders(n=5) and 14 weeks in nonresponders (n=16), and the difference in two groups was statistically significant(p$lt;0.05). The median time to progression of 14 evaluable patients was 13 weeks, and 49 weeks in the responders(n=5) and 6 weeks in the nonresponders(n=9), and the difference in two groups was statistically significant(p$lt;0.05). Myelosuppression was minimal and non-hematologic toxicities were gererally mild and well tolerated. Conclusion: The results suggest that the combination chemotherpy of AP seems to be an effective regimen for hepatocellular carcinoma. Further trials are recommended for its true efficacy.
Background/Aims: Korea is an endemic area of hepatitis B virus (HBV) infection. The routes of HBV and hepatitis C virus (HCV) infection are similar. The purposes of this study were to evaluate the effect of HBV infection on the development of anti-HCV-positive hepatocellular carcinoma (HCC) and to study the pattern of viral interaction in the patients with dual infection of HBV and HCV. Methods: One hundred thirty-seven consecutive anti-HCV-positive patients were divided into two groups: HCC group (N=58) and Non-HCC group (N=79). Various clinical, serological parameters and viral replicative status reflecting serum HBV DNA and HCV RNA positivity were compared between two groups. Results: According to multiple logistic regression analysis, male and positivity of HCV RNA, HBsAg, and HBV DNA were statistically significant variables associated with the development of HCC. The mean age at the diagnosis of HCC in the patients with dual infection was significantly younger than that of patients with HCV alone. Among 13 patients with dual infection, one third showed co-replication of HBV and HCV, but two thirds revealed only one viral replication. Conclusions: HBV infection seems to increase the risk of HCC in the anti-HCV-positive patients. To elucidate the complex profiles of viral interaction between HBV and HCV, further study may be needed.
Purpose: Tamoxifen has been well known as an effective anti-tumor agent against breast cancer. The important role of bcl-2 and p53 proteins in tamoxifen-induced apoptosis of breast cancer cells has been suggested. However, the paradoxical fact that bcl-2 over-expression is associated with better prognosis in clinic has not yet been clearly explained. To investigate this paradox, we analyzed the effect and dynamics of bcl-2 and p53 on the apoptosis after treatment of breast cancer cells with tamoxifen. Materias and Methods: The human breast cancer cell lines MCF-7 and MB MDA-468 were treated with 17- βestradiol (E2) and tamoxifen. Results: Following tamoxifen treatment, MCF-7 cells underwent apoptosis accompanied by reduced bcl-2 expression. E2 pre-treatment led to the inhibition of tamoxifen-mediated apoptosis and bcl-2 down-regulation. When MB MDA-468 cells were treated with E2 or tamoxifen, bcl-2 and p53 protein expression did not change and apoptosis did not develop. Conclusion: We observed that the down-regulation of bcl-2 by tamoxifen treatment can facilitate the apoptosis of breast cancer cells without p53 mutations. This finding was consistent with clinical experiences in which bcl-2 positive tumors were associated with more indolent phenotypes in breast cancer.
Five compounds have been isolated from the stem of Caesalpinia japonica. On the basis of spectral evidences, the structures of these compounds were identified as 4',7-dihydroxyflavone, 3,4',7-trihydroxyflavone, cathechin, 3',4',7-trihydroxyflavone and 2',3,4',5,6,7-hexahydroxyflavone.
The biochemical modulation of 5-fluorouracil(5-FU) by leucovorin has been demonstrated to enhance the activity of 5-FU in patients with advanced colorectal cancer and the synergism between 5-FU and cisplatin is well known in advanced gastrointestinal tract cancers. We conducted a phase II trial to evaluate the effect of a combination of leucovorin, 5-FU, and cisplatin(LV-FP) in patients with advanced colorectal cancer. LV-FP regimen consisted of leu- covorin 20 mg/㎡/day IV in day 1-5, 5-FU 1,000 mg/㎡/day continuous IV. infusion in day 1-5, and cisplatin 20 mg/㎡/day IV in day 1-5. The regimen was repeated every 3 weeks. Among 46 patients with histologically confirmed advanced colorectal adenocarcinoma, 31 patients had measurable lesion(s) with median age of 55 years(22-70 years). 27 patients had previous history of chemotherapy and l9 were previously untreated. There was no complete respance. 11 patients responded partially to the regimen to make the response rate 35%(l1/31). The median time to progression was 16 weeks (2-44 weeks), and the median survival time was 42 weeks(l+~80 weeks). There was no difference in response rates between the previously treated and the previously untreated. Hematologic toxicities were mild and non-hematologic toxicities were also tolerable. There was no treatment-related mortality. These results indicate that the LV-FP regimen is safe and effective in advanced colorectal adenocarcinoma.