title: Gastric mucosa alterations in first-degree relatives of gastric cancer patients.
abstract: BACKGROUND
  First-degree relatives of gastric cancer patients have an increased risk of developing such neoplasia, and several alterations in gastric mucosa of these subjects have been described. On the other hand, both gastric cell hyperproliferation and abnormalities of adhesion molecules have been involved in gastric carcinogenesis. We studied gastric mucosa alterations in first-degree relatives of gastric cancer patients.
  
  
  METHODS
  This prospective, case-controlled study enrolled 39 first-degree relatives of gastric cancer patients and 39 matched controls. Biopsy specimens obtained at endoscopy were used to assess epithelial cell proliferation plus E-cadherin and beta-catenin expression by immunohistochemical methods. H. pylori infection was assessed by histology and a rapid urease test.
  
  
  RESULTS
  Gastric epithelial cell proliferation values were not significantly different between the patient and control groups. H. pylori infection significantly increased cell proliferation values both in patients and in controls, without a significant difference between the two groups. Moreover, cell proliferation values were significantly higher in cases harboring intestinal metaplasia than in those without it. Alterations of the adhesion molecules were described exclusively in those patients harboring intestinal metaplasia. In detail, a reduction of both E-cadherin and beta-catenin expression was observed in 8 (67%) out of 12 first-degree relatives and in 6 (67%) out of 9 controls with intestinal metaplasia (p = 0.4). These alterations were similarly distributed between H. pylori infected and uninfected cases.
  
  
  CONCLUSIONS
  Our data showed that a family history of gastric cancer itself is not associated with gastric cell hyperproliferation. However, both cell hyperproliferation and alterations of adhesion molecules have been detected in those patients with intestinal metaplasia.
authors.affiliation: Oncology, Sant'Andrea Hospital, Rome, Italy. adriana.romiti@tin.it
authors.forename: Adriana
authors.initials: A
authors.lastname: Romiti
authors.forename: Angelo
authors.initials: A
authors.lastname: Zullo
authors.forename: Silverio
authors.initials: S
authors.lastname: Tomao
authors.forename: Cesare
authors.initials: C
authors.lastname: Hassan
authors.forename: Ida
authors.initials: I
authors.lastname: Sarcina
authors.forename: Vincenzo
authors.initials: V
authors.lastname: De Francesco
authors.forename: Enzo
authors.initials: E
authors.lastname: Ierardi
authors.forename: Frederica
authors.initials: F
authors.lastname: Tomao
authors.forename: Aldo
authors.initials: A
authors.lastname: Vecchione
authors.forename: Sergio
authors.initials: S
authors.lastname: Morini
mesh_terms: D015820:Cadherins / Q000096:biosynthesis; D016022:Case-Control Studies; D048708:Cell Growth Processes / Q000502:physiology; D003598:Cytoskeletal Proteins / Q000096:biosynthesis; D004847:Epithelial Cells / Q000378:metabolism / Q000473:pathology; D005192:Family Health; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism / Q000382:microbiology / Q000473:pathology*; D020022:Genetic Predisposition to Disease; D016481:Helicobacter Infections / Q000150:complications; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D013274:Stomach Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D015534:Trans-Activators / Q000096:biosynthesis; D051176:beta Catenin
chemical_list: C495270:CTNNB1 protein, human; D015820:Cadherins; D003598:Cytoskeletal Proteins; D015534:Trans-Activators; D051176:beta Catenin