Lewis blood genotypes of peptic ulcer and gastric cancer patients in Taiwan

AIM： The Lewis b （Le^b） antigen has been implicated as a possible binding site for attachment of Helicobacter pylori （H pylon） to gastric mucosa. However, studies both supporting and denying this association have been reported in the literature. Differences in secretor （Se） genotype have been suggested as a possible reason for previous discrepancies. Therefore, we investigated the relationship between Le and Se genotypes and Hpylori infection rates in people with peptic ulcer or gastric cancer. METHODS： Peripheral blood samples were obtained from 347 patients with endoscopic evidence of peptic ulcer disease （235 cases of duodenal ulcer, 62 of gastric ulcer, and 50 of combined duodenal ulcer/gastric ulcer） and 51 patients with gastric cancer on endoscopy. Peripheral blood specimens from 101 unrelated normal volunteers were used as controls. Lewis phenotype was determined using an antibody method, whereas Le and Se genotypes were determined by DNA amplification and restriction enzyme analysis. Gastric or duodenal biopsies taken from patients with endoscopic evidence of peptic ulcer or gastric cancer were cultured for Hpylotri Isolates were identified as Hpylori by morphology and production of urease and catalase. The Hpyloriinfection status was also evaluated by rapid urease test （CLO test）, and urea breath test （13^C-UBT）. Results of studies were analyzed by chi-square test （taken as significant）. RESULTS： Hpyloriwas isolated from 83.7% （303/347） of patients with peptic ulcer disease. Statistical analysis did not show any significant difference in Lewis phenotype or genotype between patients with and without Hpylori infection. No significant association was found between Lewis genotype and peptic ulcer or gastric cancer.CONCLUSION： Lewis blood genotype or phenotype may not play a role in the pathogenesis of Hpyloriinfection. However, bacterial strain differences and the presence of more than one attachment mechanism may limit the value of epidemiological studies in elucidating this matter.

Involvement of fatty acid-CoA ligase 4 in hepatocellular carcinoma growth: Roles of cyclic AMP and p38 mitogen-activated protein kinase

AIM: Fatty acid-CoA ligase 4 (FACL4) is an arachidonatepreferring enzyme which has been shown to be up-regulated in human colon cancer tissues and implicated in the colon tumorigenesis. The purpose of this study was to investigatethe role of FACL4 in the human hepatocellular carcinoma (HCC) tumorigenesis and the specific signal pathways involved in this process.METHODS: We investigated the expression and regulation of FACL4 in HCC, adjacent non-tumorous liver tissues, and cell lines.RESULTS: In HCC patients, we demonstrated that FACL4 gene expression was markedly elevated in the cancerous tissues than in the adjacent non-cancerous liver tissues.In addition, several human hepatoma cell lines, including Hep3B and HepG2, expressed high levels of FACL4. Stable overex-pression of FACL4 knockdown plasmids (small interfering RNA, siRNA) to Hep3B cells significantly decreased FACL4 expression and subsequently limited the cell proliferation. Treatment of Hep3B cells with 8bromo-cAMP and SB203508 (p38 MAPK inhibitor) significantly suppressed the FACL4 expression. CONCLUSION: FACL4 is involved in the HCC tumorigenesis and both cAMP and p38 MAPK pathways are associated with the regulation of FACL4 in HCC.