Abstract
Helicobacter pylori (HP) infection appears protective against oesophageal adenocarcinoma (EA) risk. Matrix metalloproteinases (MMPs) are released in the presence of HP infection. In MMP2 wild-type individuals, HP was significantly protective of EA risk (adjusted odds ratio: 0.29; 95% confidence interval=0.1-0.7). Matrix metalloproteinases may modulate the EA-HP relationship.
Publication types
-
Comparative Study
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adenocarcinoma / epidemiology
-
Adenocarcinoma / genetics*
-
Adenocarcinoma / virology
-
Carcinoma, Squamous Cell / epidemiology
-
Carcinoma, Squamous Cell / genetics
-
Carcinoma, Squamous Cell / virology
-
Case-Control Studies
-
Esophageal Neoplasms / epidemiology
-
Esophageal Neoplasms / genetics*
-
Esophageal Neoplasms / virology
-
Female
-
Genotype
-
Helicobacter Infections / epidemiology
-
Helicobacter Infections / genetics*
-
Helicobacter Infections / virology
-
Helicobacter pylori / genetics*
-
Helicobacter pylori / immunology
-
Humans
-
Male
-
Matrix Metalloproteinase 1 / genetics
-
Matrix Metalloproteinase 12 / genetics
-
Matrix Metalloproteinase 2 / genetics*
-
Matrix Metalloproteinase 3 / genetics
-
Middle Aged
-
Polymerase Chain Reaction
-
Polymorphism, Genetic / genetics*
-
Surveys and Questionnaires
Substances
-
Matrix Metalloproteinase 3
-
Matrix Metalloproteinase 2
-
Matrix Metalloproteinase 12
-
Matrix Metalloproteinase 1