2012
DOI: 10.1016/s0016-5085(12)61806-x
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Su1662 P53 Expression in Gastric Mucosa of Patients Infected With Helicobacter pylori

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Cited by 3 publications
(3 citation statements)
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“…Gender differences in HP-induced gastroduodenal diseases may reflect study design effects, nature of community under investigation, differences in immune responses, hormonal effects, and sex-linked genetic factors and differences in bacterial colonization [24,25]. In the present study, colonization of HP CagA+/urease + in gastric tissue was determined in 74.35% of cases versus 25.64% HP CagA−/urease + was distinguished and come in line with others [26,27]. This finding suggests that the pathogenic potential of HP strains on the gastric mucosa may be exerted in full only when …”
Section: Discussionsupporting
confidence: 89%
“…Gender differences in HP-induced gastroduodenal diseases may reflect study design effects, nature of community under investigation, differences in immune responses, hormonal effects, and sex-linked genetic factors and differences in bacterial colonization [24,25]. In the present study, colonization of HP CagA+/urease + in gastric tissue was determined in 74.35% of cases versus 25.64% HP CagA−/urease + was distinguished and come in line with others [26,27]. This finding suggests that the pathogenic potential of HP strains on the gastric mucosa may be exerted in full only when …”
Section: Discussionsupporting
confidence: 89%
“…However, the level of TP53 remained relatively low between the two peaks . In addition, a number of studies indicated that the expression of TP53 was higher in H. pylori ‐positive subjects than H. pylori ‐negative subjects, and alteration of TP53 may be an early event in H. pylori ‐associated gastric carcinogenesis . These data could be explained by the detection of mutant TP53 , which occurred in approximately 50% of all cancers .…”
Section: Discussionmentioning
confidence: 99%
“…Various studies have suggested alterations in p53 expression in pre-cancerous gastric lesions (such as atrophy or metaplasia) as efforts to stop the cycle of the damaged cell, and its build-up (lack of expression) indicates its dysfunction as a cell proliferation suppressor. Increased p53 expression may be a part of a protective mechanism against the host, arresting the cell cycle to repair the cell genome (5). The Ki67 is a nucleus antigen expressed in every cell cycle phase (except for the G0 phase).…”
Section: Introductionmentioning
confidence: 99%