H. Pylori induced G1 arrest is associated with stimulation of cyclin E/cdk2 and p21

Ashktorab, Hassan; Ahmed, Amel; Littleton, G. K.; Tackey, Robert; Walters, Curla S.; Smoot, Duane T.

doi:10.1016/s0016-5085(98)80240-0

Cited by 2 publications

(2 citation statements)

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“…In addition, Hp stimulates apoptosis in gastric epithelial cells in vitro (Wagner et al, 1997). Potential factors up‐regulating apoptosis in Hp infection include cell cycle arrest associated with p21 WAF1 induction (Ashkortab et al, 1998), Fas ligand expression by infiltrating CD45 + cells and CD95 receptor expression (Rudi et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Altered gastric epithelial cell kinetics inHelicobacter pylori-associated intestinal metaplasia: Implications for gastric carcinogenesis

et al. 2000

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We have compared apoptosis and proliferation in antral epithelium from individuals not infected with H. pylori (Hp), those with Hp-induced gastritis and those with Hp-induced gastritis containing areas of gastric intestinal metaplasia, the precursor lesion to gastric adenocarcinoma. Antral biopsies from 42 patients were assessed for evidence of Hp infection, severity of gastritis and intestinal metaplasia. Apoptosis was evaluated by the TUNEL assay and proliferation by Ki-67 immunohistochemistry and were expressed as apoptotic (AI) and proliferation (PI) indices. In the 31 Hp-positive (Hp(+)) patients, apoptosis and proliferation were increased compared with the 11 Hp-negative (Hp(-)) patients (AI = 1. 22 +/- 0.13% vs. 0.15 +/- 0.03%, p < 0.0001; PI = 24 +/- 1% vs. 13 +/- 2%, p < 0.0001). Increases were proportional to the severity of the inflammation. Within foci of intestinal metaplasia, in 9 of the Hp(+) patients, apoptosis was significantly reduced compared with surrounding gastritis (AI = 0.20 +/- 0.06% vs. 1.34 +/- 0.23%, p = 0. 0014), whereas proliferation was not altered (PI = 25.4 +/- 4% vs. 24.7 +/- 2%, p = 0.87), resulting in a lower AI/PI ratio in intestinal metaplasia than in surrounding gastritis (0.008 +/- 0.005 vs. 0.054 +/- 0.009, p < 0.02). Hp-induced gastritis is thus associated with increased epithelial apoptosis and proliferation compared with uninfected controls. In intestinal metaplasia, proliferation remains increased but apoptosis reverts to normal levels, and this perhaps contributes to Hp-associated gastric carcinogenesis.

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Section: Discussionmentioning

confidence: 99%

Altered gastric epithelial cell kinetics inHelicobacter pylori-associated intestinal metaplasia: Implications for gastric carcinogenesis

et al. 2000

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show abstract

“…In addition, Hp stimulates apoptosis in gastric epithelial cells in vitro (Wagner et al, 1997). Potential factors up-regulating apoptosis in Hp infection include cell cycle arrest associated with p21 WAF1 induction (Ashkortab et al, 1998), Fas ligand expression by infiltrating CD45 ϩ cells and CD95 receptor expression (Rudi et al, 1998).…”

Section: Apoptosis Index To Proliferation Index Ratio (Ai/pi)mentioning

confidence: 99%

Altered gastric epithelial cell kinetics in Helicobacter pylori‐associated intestinal metaplasia: Implications for gastric carcinogenesis

Scotiniotis¹,

Rokkas²,

Furth³

et al. 2000

Int. J. Cancer

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H. Pylori induced G1 arrest is associated with stimulation of cyclin E/cdk2 and p21

Cited by 2 publications

References 0 publications

Altered gastric epithelial cell kinetics inHelicobacter pylori-associated intestinal metaplasia: Implications for gastric carcinogenesis

Altered gastric epithelial cell kinetics inHelicobacter pylori-associated intestinal metaplasia: Implications for gastric carcinogenesis

Altered gastric epithelial cell kinetics in Helicobacter pylori‐associated intestinal metaplasia: Implications for gastric carcinogenesis

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