Karaman A, Kabalar M Eşref, Binici D Nasir, Oztürk C, Pirim I
Department of Medical Genetics, Erzurum Nenehatun Obstetrics and Gynecology Hospital, Erzurum, Turkey.
Genet Couns. 2010;21(4):439-50.
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.
为研究胃癌前病变（GPL）中17号染色体短臂（p53）杂合性缺失（LOH）及四倍体或非整倍体增加的情况，以及它们与幽门螺杆菌（H pylori）感染的关系。共研究了78份胃黏膜活检标本，包括10份正常黏膜和68份胃癌前病变[慢性萎缩性胃炎（CAG，n = 20）、肠化生（IM，n = 12）、低级别上皮内瘤变（LGD，n = 15）和高级别上皮内瘤变（HGD，n = 21）]，采用聚合酶链反应（PCR）和流式细胞术进行检测。采用改良吉姆萨染色技术检测H pylori。该研究于2007年至2009年在埃尔祖鲁姆努穆内医院进行。在CAG中，17p（p53）LOH的发生率为（1/20）5%；在IM中为（2/12）16%；在LGD中为（3/15）20%；在HGD中为（11/21）53%。17p（p53）LOH的发生率与GPL的组织学类型之间存在相关性（P = 0.004）。同样，在CAG中，四倍体或非整倍体增加的发生率为（1/20）5%；在IM中为（1/12）8%；在LGD中为（2/15）13%；在HGD中为（9/21）43%。非整倍体与GPL的组织学类型之间存在相关性（P = 0.009）。然而，GPL的组织学类型与H pylori感染的存在之间没有相关性（P = 0.921）。另一方面，在所有GPL中，四倍体或非整倍体增加与17p（p53）LOH之间存在显著相关性（P = 0.0001）。然而，GPL中H pylori感染与17p（p53）LOH或四倍体/非整倍体增加之间没有统计学上的显著相关性。17p（p53）LOH以及四倍体或非整倍体增加与胃癌发生的早期阶段密切相关。
