AIM: To answer the question whether FHIT gene expression is affected by the family history of gastric carcinoma and the presence of Helicobacter pylori (H pylori) in the gastric mucosa of patients with dyspepsia. METHODS: FHIT gene expression in two different topographic sites of the gastric mucosa of twenty-one patients with dyspepsia and with or without familial gastric carcinoma, infected or not infected with H pylori, was evaluated by reverse transcription-PCR (RT-PCR) and IMAGE QUANT methods. A rapid urease test and histopathological examination were used to determine H pylori colonization. RESULTS: In the gastric mucosa of patients with family histories of gastric carcinoma, the amount of FHIT protein mRNA was reduced down to 32%, and for patients with H pylori colonization, to 24% in comparison to controls with dyspepsia and without cancer in the family. FHIT expression was independent of the topography of specimens (corpus vs antrum), and for the control patients it was less sensitive to infection with H pylori. A considerable statistical difference in FHIT levels was observed in the gastric mucosa from the corpus of patients with family histories of gastric carcinoma in respect to H pylori colonization (P = 0.06). Macroscopic evaluation of the gastric mucosa demonstrated that pathologic changes classified according to the Sydney system had no significant influence on FHIT expression within each tested group of patients. CONCLUSION: Loss of FHIT expression was observed in patients with dyspepsia and family histories of gastric carcinoma, especially those infected with H pylori. Such results may constitute an early indication of the development of gastric carcinoma, which is associated with family factors including heredity and H pylori infection. The loss of the FHIT gene may serve as a marker for early diagnosis and prevention of gastric carcinoma, especially in context of early monitoring of H pylori infection in individuals with a record of familial stomach cancer.
AIM: To answer the question whether FHIT gene expression is affected by the family history of gastric carcinoma and the presence of Helicobacter pylori (H pylori) in the gastric mucosa of patients with dyspepsia. METHODS:FHIT gene expression in two different topographic sites of the gastric mucosa of twenty-one patients with dyspepsia and with or without familial gastric carcinoma, infected or not infected with H pylori, was evaluated by reverse transcription-PCR (RT-PCR) and IMAGE QUANT methods. A rapid urease test and histopathological examination were used to determine H pylori colonization. RESULTS: In the gastric mucosa of patients with family histories of gastric carcinoma, the amount of FHIT protein mRNA was reduced down to 32%, and for patients with H pylori colonization, to 24% in comparison to controls with dyspepsia and without cancer in the family. FHIT expression was independent of the topography of specimens (corpus vs antrum), and for the control patients it was less sensitive to infection with H pylori. A considerable statistical difference in FHIT levels was observed in the gastric mucosa from the corpus of patients with family histories of gastric carcinoma in respect to H pylori colonization (P = 0.06). Macroscopic evaluation of the gastric mucosa demonstrated that pathologic changes classified according to the Sydney system had no significant influence on FHIT expression within each tested group of patients. CONCLUSION: Loss of FHIT expression was observed in patients with dyspepsia and family histories of gastric carcinoma, especially those infected with H pylori. Such results may constitute an early indication of the development of gastric carcinoma, which is associated with family factors including heredity and H pylori infection. The loss of the FHIT gene may serve as a marker for early diagnosis and prevention of gastric carcinoma, especially in context of early monitoring of H pylori infection in individuals with a record of familial stomach cancer.
Authors: F R Khuri; J Nemunaitis; I Ganly; J Arseneau; I F Tannock; L Romel; M Gore; J Ironside; R H MacDougall; C Heise; B Randlev; A M Gillenwater; P Bruso; S B Kaye; W K Hong; D H Kirn Journal: Nat Med Date: 2000-08 Impact factor: 53.440
Authors: H Ishii; K R Dumon; A Vecchione; F Trapasso; K Mimori; H Alder; M Mori; G Sozzi; R Baffa; K Huebner; C M Croce Journal: Cancer Res Date: 2001-02-15 Impact factor: 12.701
Authors: S H Lee; W H Kim; H K Kim; K M Woo; H S Nam; H S Kim; J G Kim; M H Cho Journal: Biochem Biophys Res Commun Date: 2001-06-15 Impact factor: 3.575
Authors: P C Konturek; S J Konturek; T Starzyska; K Marlicz; W Bielanski; P Pierzchalski; E Karczewska; A Hartwich; K Rembiasz; M Lawniczak; W Ziemniak; E C Hahn Journal: Aliment Pharmacol Ther Date: 2000-10 Impact factor: 8.171
Authors: Emma Bragantini; Stefano Barbi; Stefania Beghelli; Patrick S Moore; Giovanni de Manzoni; Franco Roviello; Anna Tomezzoli; Carla Vindigni; Raffaele Baffa; Aldo Scarpa Journal: J Cancer Res Clin Oncol Date: 2005-10-11 Impact factor: 4.553