AIMS: Intestinal metaplasia is considered to be a precursor lesion in both Barrett's and intestinal-type gastric cancer. The aim was to clarify the differences in molecular pathology between specialized intestinal metaplasia (SIM) in Barrett's oesophagus (BO), cardiac (CIM) and gastric intestinal metaplasia (GIM). METHODS AND RESULTS: Eighty-eight SIM cases with BO, 30 CIM cases and 52 GIM cases in patients with or without Helicobacter pylori infectionwere analysed for genetic instability and Das-1. Microsatellite instability and a loss of heterozygosity were evaluated at five microsatellite loci. The incidence of genetic instability was 55.7% in SIM, 40.0% in CIM and 23.1% in GIM, revealing a significant difference between SIM and GIM (P < 0.0005). For each microsatellite marker analysed, there were obvious differences in frequency among the three conditions. Das-1 reactivity was significantly higher in SIM than in CIM or GIM (P < 0.0001, both). Interestingly, both genetic instability and Das-1 reactivity in SIM showed a significantly higher incidence in patients with H. pylori infection than in those without (P < 0.005 and P < 0.01, respectively). CONCLUSIONS: SIM is distinct from CIM and GIM, and the pathogenesis of SIM, like that of GIM, is associated to some degree with H. pylori infection in a Japanese population.
AIMS: Intestinal metaplasia is considered to be a precursor lesion in both Barrett's and intestinal-type gastric cancer. The aim was to clarify the differences in molecular pathology between specialized intestinal metaplasia (SIM) in Barrett's oesophagus (BO), cardiac (CIM) and gastric intestinal metaplasia (GIM). METHODS AND RESULTS: Eighty-eight SIM cases with BO, 30 CIM cases and 52 GIM cases in patients with or without Helicobacter pylori infectionwere analysed for genetic instability and Das-1. Microsatellite instability and a loss of heterozygosity were evaluated at five microsatellite loci. The incidence of genetic instability was 55.7% in SIM, 40.0% in CIM and 23.1% in GIM, revealing a significant difference between SIM and GIM (P < 0.0005). For each microsatellite marker analysed, there were obvious differences in frequency among the three conditions. Das-1 reactivity was significantly higher in SIM than in CIM or GIM (P < 0.0001, both). Interestingly, both genetic instability and Das-1 reactivity in SIM showed a significantly higher incidence in patients with H. pylori infection than in those without (P < 0.005 and P < 0.01, respectively). CONCLUSIONS: SIM is distinct from CIM and GIM, and the pathogenesis of SIM, like that of GIM, is associated to some degree with H. pylori infection in a Japanese population.
Authors: Lori A Fischbach; Helena Nordenstedt; Jennifer R Kramer; Subi Gandhi; Sam Dick-Onuoha; Anthony Lewis; Hashem B El-Serag Journal: Helicobacter Date: 2012-03-20 Impact factor: 5.753
Authors: Shane P Duggan; Fiona M Behan; Murat Kirca; Abdul Zaheer; Sarah A McGarrigle; John V Reynolds; Gisela M F Vaz; Mathias O Senge; Dermot Kelleher Journal: Sci Rep Date: 2016-09-02 Impact factor: 4.379
Authors: Bálint Erőss; Nelli Farkas; Áron Vincze; Benedek Tinusz; László Szapáry; András Garami; Márta Balaskó; Patrícia Sarlós; László Czopf; Hussain Alizadeh; Zoltán Rakonczay; Tamás Habon; Péter Hegyi Journal: Helicobacter Date: 2018-06-25 Impact factor: 5.753