Helicobacter · 2009
Helicobacter pylori infection and family history of gastric cancer decrease expression of FHIT tumor suppressor gene in gastric mucosa of dyspeptic patients.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Stec-Michalska Krystyna, Peczek Lukasz, Michalski Blazej, Wisniewska-Jarosinska Maria, Krakowiak Agnieszka, Nawrot Barbara
Аннотация
BACKGROUND: The expression of a fragile histidine triad (FHIT) protein is lost in stomach tumors. The study aimed at determining whether FHIT expression is affected by Helicobacter pylori infection, strain virulence (vacA and cagA genes) and histopathological changes in the gastric mucosa of patients with functional dyspepsia having first-degree relatives with gastric cancer.
MATERIALS AND METHODS: Eighty-eight never-smoking patients with functional dyspepsia were selected for the study, and 48 of them had first-degree relatives with gastric cancer. Bacterial DNA amplification was used to identify H. pylori colonization. The level of FHIT gene expression was determined by qRT-PCR (mRNA) and Western blot (FHIT protein) analyses.
RESULTS: For patients having first-degree relatives with gastric cancer FHIT expression was lower (mRNA by ca. 40-45% and protein by 30%) compared with the control patients (p < .05). H. pylori infection decreased the FHIT mRNA level by 10-35% and the protein level by 10-20%. Bacterial strain vacA(+)cagA(+) lowered FHIT mRNA by ca. 30-35% in the antrum samples of both groups and in corpus samples of patients with first-degree relatives with gastric cancer (p < .05). The FHIT mRNA level was twice as high in control H. pylori-negative patients with intestinal metaplasia, compared with those with non-atrophic gastritis.
CONCLUSIONS: The decreased FHIT gene expression associated with hereditary factors and with H. pylori infection, especially with vacA(+)cagA(+)-positive strains, may be related to gastric carcinoma development.
MATERIALS AND METHODS: Eighty-eight never-smoking patients with functional dyspepsia were selected for the study, and 48 of them had first-degree relatives with gastric cancer. Bacterial DNA amplification was used to identify H. pylori colonization. The level of FHIT gene expression was determined by qRT-PCR (mRNA) and Western blot (FHIT protein) analyses.
RESULTS: For patients having first-degree relatives with gastric cancer FHIT expression was lower (mRNA by ca. 40-45% and protein by 30%) compared with the control patients (p < .05). H. pylori infection decreased the FHIT mRNA level by 10-35% and the protein level by 10-20%. Bacterial strain vacA(+)cagA(+) lowered FHIT mRNA by ca. 30-35% in the antrum samples of both groups and in corpus samples of patients with first-degree relatives with gastric cancer (p < .05). The FHIT mRNA level was twice as high in control H. pylori-negative patients with intestinal metaplasia, compared with those with non-atrophic gastritis.
CONCLUSIONS: The decreased FHIT gene expression associated with hereditary factors and with H. pylori infection, especially with vacA(+)cagA(+)-positive strains, may be related to gastric carcinoma development.