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Alteraciones genéticas en gastritis crónica: Estudio de inestabilidad microsatelital y pérdida de la heterocigocidad / Genetic changes in chronic gastritis: study of microsatellite instability and loss of heterozygosity
Roa S, Juan Carlos; Villaseca V, Miguel Angel; Roa E, Iván; Araya O, Juan Carlos.
  • Roa S, Juan Carlos; Universidad de La Frontera. Facultad de Medicina. Departamento de Anatomía Patológica. Temuco. CL
  • Villaseca V, Miguel Angel; Universidad de La Frontera. Facultad de Medicina. Departamento de Anatomía Patológica. Temuco. CL
  • Roa E, Iván; Universidad de La Frontera. Facultad de Medicina. Departamento de Anatomía Patológica. Temuco. CL
  • Araya O, Juan Carlos; Universidad de La Frontera. Facultad de Medicina. Departamento de Anatomía Patológica. Temuco. CL
Rev. méd. Chile ; 131(12): 1365-1374, dic. 2003. ilus, tab
Article in Spanish | LILACS | ID: lil-360233
ABSTRACT
Background: Multifocal chronic gastritis, associated to intestinal metaplasia, is considered a preneoplastic lesion, closely associated to intestinal type gastric cancer. Aim: To study the frequency of microsatellite instability (MSI) and loss of heterozygosity (LOH) in areas of chronic gastritis and intestinal metaplasia in gastric biopsies of patients without cancer. Material and methods: Gastric biopsy samples from 34 patients without cancer (22 with multifocal atrophic gastritis and 12 with diffuse antral gastritis), were studied. Glands from areas of chonic gastritis and intestinal metaplasia and lymphocytes, were collected using laser microdissection of paraffin embedded samples. The analysis of 15 mono and dinucleotide microsatellites was used to assess LOH and MSI. Results: LOH and MSI were found in some of the markers in 55% (12/22) and 59% (13/22) of cases with intestinal metaplasia, respectively. Only one of 12 areas with diffuse atrophic gastritis had MSI and a different area had LOH (p <0.05 or less, when compared with areas of multifocal atrophic gastritis). Three areas of normal epithelium in patients with multifocal atrophic gastritis, also had alterations. Most of these alterations were concordant with adjacent areas with intestinal metaplasia. Conclusions: LOH and MSI was found in areas of intestinal metaplasia in more than half of the studied cases and in few areas of atrophic gastritis without intestinal metaplasia. These findings suggest that genotypic alterations may precede phenotypic modifications and that intestinal metaplasia is a preneoplastic lesion (Rev Méd Chile 2003; 131: 1365-74).
Subject(s)
Full text: Available Index: LILACS (Americas) Main subject: Microsatellite Repeats / Loss of Heterozygosity / Gastritis / Intestines Limits: Humans Language: Spanish Journal: Rev. méd. Chile Journal subject: Medicine Year: 2003 Type: Article / Project document Affiliation country: Chile Institution/Affiliation country: Universidad de La Frontera/CL

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Full text: Available Index: LILACS (Americas) Main subject: Microsatellite Repeats / Loss of Heterozygosity / Gastritis / Intestines Limits: Humans Language: Spanish Journal: Rev. méd. Chile Journal subject: Medicine Year: 2003 Type: Article / Project document Affiliation country: Chile Institution/Affiliation country: Universidad de La Frontera/CL