Akademik Veri Yönetim Sistemi
GENETIC COUNSELING, cilt.21, sa.4, ss.439-450, 2010 (SCI-Expanded, Scopus)
Genetic alterations in gastric precancerous lesions: To investigate the occurrence of 17p(p53) loss of heterozygosity (LOH) and increased 4N or aneuploidy in gastric precancerous lesions (GPL), and their association with Helicobacter pylori (H pylori) infection. A total of 78 gastric mucosal biopsy specimens, including 10 normal mucosa and 68 gastric precancerous lesions [chronic atrophic gastritis (CAG, n=20), intestinal metaplasia (IM, n=12), low grade dysplasia (LGD, n=15), and high grade dysplasia (HGD, n=21)] were studied using PCR and flow cytometry. A modified Giemsa staining technique was used to detect H pylori. The study was performed in Erzurum Numune Hospital between 2007 and 2009. 17p(p53)LOH was observed in (1/20) 5% of CAG, in (2/12) 16% of IM, in (3/15) 20% of LGD and in (11/21) 53% of HGD. There was correlation between prevalence of 17p(p53) LOH and histological type of GPL (P=0.004). Similarly, increased 4N or aneuploidy was detected in (1/20) 5% of CAG, in (1/12) 8% of IM, in (2/15) 13% of LGD and in (9/21)43% of HGD. The correlation was found between aneuploidy and histological type of GPL (P=0.009). However, there was no correlation between presence of H pylori infection in histological type of GPL (P=0.921). On the other hand, a significant association was found between increased 4N or aneuploidy and 17p(p53)LOH in all of GPL (P=0.0001). However, there was no statistically significant association between H pylori infection and 17p(p53)LOH or increased 4N/ aneuplody in GPL. 17p(p53) LOH and increased 4N or aneuploidy are closely related to the early stages of gastric carcinogenesis.