Caga-positive strains of Helicobacter pylori may protect against Barrett’s esophagus

[1]  S. Hazell,et al.  Serological response to specific Helicobacter pylori antigens: antibody against CagA antigen is not predictive of gastric cancer in a developing country. , 1996, The American journal of gastroenterology.

[2]  E. Kuipers,et al.  Increase of Helicobacter pylori-associated corpus gastritis during acid suppressive therapy: implications for long-term safety. , 1995, The American journal of gastroenterology.

[3]  S. Spechler,et al.  The increasing frequency of adenocarcinoma of the esophagus , 1989, Cancer.

[4]  Chi-Sen Chang,et al.  The incidence of reflux esophagitis among the Chinese. , 1997, The American journal of gastroenterology.

[5]  M. Blaser,et al.  Correlation of H. pylori-related Cag a with severity of fundic gastritis and gastric secretion , 1998 .

[6]  E. El-Omar,et al.  Helicobacter pylori infection and chronic gastric acid hyposecretion. , 1997, Gastroenterology.

[7]  M. Blaser,et al.  The seroprevalence of cagA-positive Helicobacter pylori strains in the spectrum of gastroesophageal reflux disease. , 1998, Gastroenterology.

[8]  E. El-Omar,et al.  Helicobacter pylori infection and abnormalities of acid secretion in patients with duodenal ulcer disease. , 1995, Gastroenterology.

[9]  M. Blaser Helicobacter pylori phenotypes associated with peptic ulceration. , 1994, Scandinavian journal of gastroenterology. Supplement.

[10]  D. Graham,et al.  Epidemiology of Helicobacter pylori in an asymptomatic population in the United States. Effect of age, race, and socioeconomic status. , 1991, Gastroenterology.

[11]  T. Jørgensen,et al.  Epidemiology of upper dyspepsia in a random population. Prevalence, incidence, natural history, and risk factors. , 1994, Scandinavian journal of gastroenterology.

[12]  M. Blaser,et al.  Heightened inflammatory response and cytokine expression in vivo to cagA+ Helicobacter pylori strains. , 1995, Laboratory investigation; a journal of technical methods and pathology.

[13]  E. Kuipers,et al.  Helicobacter pylori and atrophic gastritis: importance of the cagA status. , 1996, Journal of the National Cancer Institute.

[14]  M F Dixon,et al.  Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. , 1996, The American journal of surgical pathology.

[15]  M. Blaser,et al.  Infection with Helicobacter pylori strains possessing cagA is associated with an increased risk of developing adenocarcinoma of the stomach. , 1995, Cancer research.

[16]  A B West,et al.  An inverse relation between cagA+ strains of Helicobacter pylori infection and risk of esophageal and gastric cardia adenocarcinoma. , 1998, Cancer research.

[17]  M. Blaser,et al.  Serologic detection of infection with cagA+ Helicobacter pylori strains , 1995, Journal of clinical microbiology.

[18]  A. Blum,et al.  Curing Helicobacter pylori infection in patients with duodenal ulcer may provoke reflux esophagitis. , 1997, Gastroenterology.

[19]  G Van Belle,et al.  Observer variation in the diagnosis of dysplasia in Barrett's esophagus. , 1988, Human pathology.

[20]  M. Blaser,et al.  The seroprevalence of -positive strains in the spectrum of gastroesophageal reflux disease , 1998 .