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AIM:To examine the expression of nuclear factor kappaB(NF-xB) and its target genes in intestinal metaplasia (IM),dysplasia (DYS) and gastric carcinoma (GC) infected withHelicobacter pylori (H pylori) and to investigate themechanism underlying Hpyloricytotoxin associated gene A(cag A) infection leading to gastric adenocarcinoma.METHODS:Expressions of NF-kB/p65 and its target genes:c-myc,cyclinD1 and bcl-xl were immunohistochemicallyexamined in 289 cases of gastric biopsy and resectionspecimens from patients with IM,DYS and GC infected withH pylori.H pylori in the above mentioned tissues wasdetected by Warthin-Starry stain and rapid urease tests.IgG antibody to cagA in sera of the patients was measuredby ELISA.RESULTS:The positive rates of NF-kB/p65 were significantlyhigher in groups with cagA of IMⅠ-Ⅱ(28/33),IMⅢ(48/52),DYSI(27/31),DYS Ⅱ-Ⅲ(28/32),GC(35/40) than in groupswithout cagA of IMⅠ-Ⅱ(4/17),IMⅢ(3/20),DYSI(3/20),DYSⅡ-Ⅲ(6/21),GC(10/23).The expressions of c-myc,cyclinD1,and bcl-xl were significantly higher in groups withcagA of IM Ⅲ(47/52,49/52,46/52),DYSⅡ-Ⅲ(29/32,26/32,25/32) than in groups without cagA of IM Ⅲ(8/20,7/20,5/20),DYSⅡ-Ⅲ(10/21,8/21,3/21),which were in conformitywith the expression of NF-kB in IM Ⅲ,and DYSⅡ-Ⅲ.Asignificantly higher expression level of NF-kB/p65,c-myc,cyclinD1 and bcl-xl was detected in intestinal type GC(27/28,18/28,22/28,24/28) than in diffuse type GC(8/12,3/12,3/12,6/12),respectively.CONCLUSION:There may be two different molecularmechanisms in the occurrence of intestinal and diffuse typegastric carcinomas,intestinal type gastric carcinoma isstrongly associated with high expression of c-myc,cyclinD1and bcl-xl through NF-kB/p65 activated by Hpylori cagA.inhibiting the activity of NF-kB is an effective and promisingway to prevent intestinal type gastric carcinoma.
AIM: To examine the expression of nuclear factor kappaB (NF-xB) and its target genes in intestinal metaplasia (IM), dysplasia (DYS) and gastric carcinoma (GC) infected withHelicobacter pylori (H pylori) and to investigate themechanism underlying Hpyloricytotoxin associated gene A (cag A) infection leading to gastric adenocarcinoma. METHODS: Expressions of NF-kB / p65 and its target genes: c-myc, cyclinD1 and bcl-xl were immunohistochemically modified in 289 cases of gastric biopsy and resectionspecimens from patients with IM, DYS and GC infected with H pylori. H pylori in the above mentioned tissues was detected by Warthin-Starry stain and rapid urease tests. IgG antibody to cagA in sera of the patients was measured by ELISA .RESULTS: The positive rates of NF-kB / p65 were significantlyhigher in groups with cagA of IMⅠ-Ⅱ (28/33), IMⅢ (48/52), DYSI (27/31), DYSⅡ-Ⅲ (28/32), GC The expressions of c-myc, cy (4/17), IMⅢ (3/20), DYSI (3/20), DYSⅡ-Ⅲ clinD1, and bcl-xl were significantly higher in groups with cagA of IM III (47/52, 49/52, 46/52), DYSⅡ-Ⅲ (29/32, 26/32, 25/32) than in groups without cagA of IM III (8/20, 7/20, 5/20), DYSII-III (10/21, 8/21, 3/21), which were in conformity with the expression of NF-kB in IM III, and DYS II -Ⅲ.Asignificantly higher expression level of NF-kB / p65, c-myc, cyclinD1 and bcl-xl was detected in intestinal type GC (27/28, 18/28, 22/28, 24/28) than in diffuse type GC (8/12, 3/12, 3/12, 6/12), respectively. CONCLUSION: There may be two different molecular mechanisms in the occurrence of intestinal and diffuse type gastric carcinomas, intestinal type gastric carcinoma isstrongly associated with high expression of c -myc, cyclinD1and bcl-xl through NF-kB / p65 activated by Hpylori cagA. inhibits the activity of NF-kB is an effective and promisingway to prevent intestinal type gastric carcinoma.