Genetic alterations in gastric precancerous lesions.

摘要: Summary: Genetic alterations in gastric precaneemus lesiona: To investigate the occurrence of 1 7p(p53) loss heterozygosity (LOH) and increased 4N or aneuploidy precancerous lesions (GPL), their association with llelicohacter pvlori (Il pylori) inl'ection. A total 78 mucosa! biopsy specimens, including 10 normal mucosa 68 [chronic atrophie gastritis (CA(J, n=20), intestinal metaplasia (IM, ?=?2), low grade dysplasia (L(JD, n=l5), high (HGD, n=21)] were studied using PCR flow cytometry. modified (iiemsa staining technique was used to detect H pylori. The study performed Erzurum Nuinune Hospital between 2007 20(W. l7p(p53)LOH observed (1/20) 5% CAG, ( 2/12) 16% oflM, (3/15) 20% LCD 1/ 21 ) 53% HGD. There correlation prevalence LOH hislologieal type GPL (/>=0.004). Similarly, detected 1/20) 5%, I/ 2) 8% IM, (2/15) 13% LGD (9/21 43% found histologica! (/>=0.0(I9). However, there no presence pylori infection (/>=0.921). On other hand, a significant 7p(p53)LOH all (P=(LOOOI ). statistically // 4N/ aneuplody GPL. I7p(p53) are closely related early stages carcinogenesis. Key-words: p53 gene - Loss helerozygosity Aneuploidy Helicobacter Gastric lesions. INTRODUCTION development cancer humans has been shown be multistep process, ranging from chronic atrophy, metaplasia, finally (7, 53, 59). In process carcinogenesis, bacterium plays major etiological role recently classified as type-I carcinogen (17). is generally believed initial trigger cascade this beginning active inflammatory response mucosae subsequently progressing ultimately (8). Mutation allelic deletion appears play an important human carcinoma (16, 18, 41). It established that accumulation wild-type protein results two pathways; cell cycle arrest programmed death, which together involved tumor suppressor functions (19). Therefore mutation leads disruption these pathways, selective growth advantage for cells function may result proliferation activity (60). control prevents DNA breaks entering synthesis where could replicated cause chromosome damage lead progressive genetic instability (27). located at 17pl3 (15). Inactivation involves two-step mechanism consisting point on one aliele, consistent Knudson's two-hit hypothesis. One copy typically inactivated by mutation, whereas second lost called 7p (LOH). p53+/+ respond genotoxic injury undergoing death. p53-/- do not continue proliferate, accumulating (3, 19, 38). Cell populations making up present morphologic functional features vary time different stimuli. …