AIM:To examine the expression of nuclear factor kappaB (NF-κB) and its target genes in intestinal metaplasia (IM),dysplasia (DYS) and gastric carcinoma (GC) infected with Helicobacter pylori (H pylori) and to investi...AIM:To examine the expression of nuclear factor kappaB (NF-κB) and its target genes in intestinal metaplasia (IM),dysplasia (DYS) and gastric carcinoma (GC) infected with Helicobacter pylori (H pylori) and to investigate the mechanism underlying Hpyloricytotoxin associated gene A(cag A) infection leading to gastric adenocarcinoma.METHODS: Expressions of NF-κB/p65 and its target genes:c-myc, cyclinD1 and bcl-xl were immunohistochemically examined in 289 cases of gastric biopsy and resection specimens 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-κB/p65 were significantly higher in groups with cagA of IMI-Ⅱ(28/33), IM III(48/52),DYSI(27/31), DY5 Ⅱ-Ⅲ(28/32), GC(35/40) than in groups without 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 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-κB in IM Ⅲ, and DYSⅡ-Ⅲ. Asignificantly higher expression level of NF-κB/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 is strongly associated with high expression of c-myc, cyclinD1 and bcl-xl through NF-κB/p65 activated by Hpylori cagA.Inhibiting the activity of NF-κB is an effective and promising way to prevent intestinal type gastric carcinoma.展开更多
AIM: To elucidate the role and alterations of syndecan-1 and E-cadherin expression in different cellular phenotypes of differentiated-type gastric cancers (DGCs), METHODS: A total of 120 DGCs at an early stage, andthe...AIM: To elucidate the role and alterations of syndecan-1 and E-cadherin expression in different cellular phenotypes of differentiated-type gastric cancers (DGCs), METHODS: A total of 120 DGCs at an early stage, andtheir adjacent mucosa, were studied both by immunohistochemistry. Syndecan-1 and E-cadherin were assessed by immunohistochemical staining with anti-syndecan-1 and anti-E-cadherin antibodies, respectively. Based on immunohistochemistry, DGCs and their surrounding mucosa were divided into four types: gastric type (G-type),ordinary type (O-type), complete-intestinal type (CI-type),and null type (N-type).RESULTS: Syndecan-1 expression was significantly lower in G-type cancers (29.4%) than in O-type (79.6%) and CI-type cancers (90%) (P＜0.05, respectively), but E-cadherin did not show this result. In addition, syndecan-1 expression was significantly reduced in DGCs comprised partly of poorly differentiated adenocarcinoma or signet-ring cell carcinoma, compared to DGCs demonstrating papillary and/or tubular adenocarcinoma (P＜0.05). G-type intestinal metaplasia (IM) surrounding the tumors was observed in 23.8% of G-type, 4.9% of O-type, and 6.7% of CI-type cancers (P＜0.05; G-type vs O-type). Reduction of syndecan-1 expression was significant in G-type IM (25%) compared to non-G-type IM (75%; P＜0.05).CONCLUSION: Loss of syndecan-1 plays a role in the growth of G-type cancers of DGCs at an early stage, and the reduction of syndecan-1 expression in IM surrounding the tumors may influence the growth of G-type cancer.展开更多
基金Supported by grants from the Bureau of Science and Technology of Hubei Province,No.2003AA301C27
文摘AIM:To examine the expression of nuclear factor kappaB (NF-κB) and its target genes in intestinal metaplasia (IM),dysplasia (DYS) and gastric carcinoma (GC) infected with Helicobacter pylori (H pylori) and to investigate the mechanism underlying Hpyloricytotoxin associated gene A(cag A) infection leading to gastric adenocarcinoma.METHODS: Expressions of NF-κB/p65 and its target genes:c-myc, cyclinD1 and bcl-xl were immunohistochemically examined in 289 cases of gastric biopsy and resection specimens 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-κB/p65 were significantly higher in groups with cagA of IMI-Ⅱ(28/33), IM III(48/52),DYSI(27/31), DY5 Ⅱ-Ⅲ(28/32), GC(35/40) than in groups without 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 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-κB in IM Ⅲ, and DYSⅡ-Ⅲ. Asignificantly higher expression level of NF-κB/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 is strongly associated with high expression of c-myc, cyclinD1 and bcl-xl through NF-κB/p65 activated by Hpylori cagA.Inhibiting the activity of NF-κB is an effective and promising way to prevent intestinal type gastric carcinoma.
基金Supported by the Medical Science Research Foundation of Hubei Province, No. 101130780
文摘AIM: To elucidate the role and alterations of syndecan-1 and E-cadherin expression in different cellular phenotypes of differentiated-type gastric cancers (DGCs), METHODS: A total of 120 DGCs at an early stage, andtheir adjacent mucosa, were studied both by immunohistochemistry. Syndecan-1 and E-cadherin were assessed by immunohistochemical staining with anti-syndecan-1 and anti-E-cadherin antibodies, respectively. Based on immunohistochemistry, DGCs and their surrounding mucosa were divided into four types: gastric type (G-type),ordinary type (O-type), complete-intestinal type (CI-type),and null type (N-type).RESULTS: Syndecan-1 expression was significantly lower in G-type cancers (29.4%) than in O-type (79.6%) and CI-type cancers (90%) (P＜0.05, respectively), but E-cadherin did not show this result. In addition, syndecan-1 expression was significantly reduced in DGCs comprised partly of poorly differentiated adenocarcinoma or signet-ring cell carcinoma, compared to DGCs demonstrating papillary and/or tubular adenocarcinoma (P＜0.05). G-type intestinal metaplasia (IM) surrounding the tumors was observed in 23.8% of G-type, 4.9% of O-type, and 6.7% of CI-type cancers (P＜0.05; G-type vs O-type). Reduction of syndecan-1 expression was significant in G-type IM (25%) compared to non-G-type IM (75%; P＜0.05).CONCLUSION: Loss of syndecan-1 plays a role in the growth of G-type cancers of DGCs at an early stage, and the reduction of syndecan-1 expression in IM surrounding the tumors may influence the growth of G-type cancer.
