Original ContributionsEpstein-Barr virus, p53 protein, and microsatellite instability in the adenoma-carcinoma sequence of the stomach*,**
Section snippets
Specimens
Sixty-six surgically resected stomachs with a gastric adenoma focus adjacent to or within gastric carcinoma (Fig 1), 81 cases of simple gastric adenomas (without carcinoma), and 306 cases of de novo gastric carcinoma (without adenoma focus) were retrospectively identified from the surgical pathology files of Seoul National University Hospital.
Clinicopathologic comparison between adenoma-carcinoma cases, simple adenomas, and de novo carcinomas
Clinicopathologic features are summarized in Table 1.Empty Cell Adenoma-Carcinoma Sequence (n = 66) Empty Cell Empty Cell Empty Cell Empty Cell Adenomas Carcinomas Simple Adenomas (n = 81) De Novo Carcinomas (n = 306) P Value Patients Age Mean 61.44 years 60.22 years 54.49 years Range 42–86 year 28–82 years 18–80 years Male:Female ratio 50:16 66:15 208:98 Adenomas Histology Tubular 49 69 Not significant Villotubular 10 10 Villous 7 2 Grade High 30 23 0.03 Low 36 58
Discussion
The present study is the first to demonstrate that EBV incorporation is not possibly associated with the gastric adenoma-carcinoma sequence and to suggest that transcriptional activation of EBV probably occurs relatively late (after the adenoma stage) in the gastric adenoma-carcinoma sequence, although it still remains unknown in case of gastric cancer unrelated to the adenoma-carcinoma sequence. In the present study, the cases of gastric carcinomas within or adjacent to adenomas (ie,
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Cited by (18)
Gastric epithelial dysplasia: The Western perspective
2008, Digestive and Liver DiseaseCitation Excerpt :APC gene is mutated in 20–76% of gastric adenomas and flat dysplasias and nuclear p53 staining may be seen in about one third of these cases [63–68]. TP53 mutations have also been described in H. pylori gastritis and in foci of intestinal metaplasia suggesting these are early events in gastric carcinogenesis [69–81]. Microsatellite instability (MSI) may occur in about 21% of gastric adenomas, [65,71,76,82–87] while the exact role of KRAS oncogene mutation in gastric neoplasia is debatable [65,66,69,82,88,89].
Gastric Preneoplastic Lesions and Epithelial Dysplasia
2007, Gastroenterology Clinics of North AmericaCitation Excerpt :p53 mutations are detected in 30% to 50% of gastric carcinomas [110,111]. Immunohistochemical studies have shown p53 nuclear staining in about one third of cases of gastric dysplasias or adenomas [110–118], usually, but not invariably, limited to areas of high-grade dysplasia [112,115,116,118,119]. Interestingly, p53 mutations also have been detected (by immunohistochemistry or molecular techniques) in H pylori gastritis and intestinal metaplasia (approximately 30%), indicating that p53 alterations may be an early event in gastric carcinogenesis [120–122].
Epstein-Barr virus associated gastric dysplasia: a new rare entity?
2022, Virchows ArchivClinicopathologic characteristics of microsatellite instable gastric carcinomas revisited: Urgent need for standardization
2017, Applied Immunohistochemistry and Molecular MorphologyMicrosatellite instability of nuclear and mitochondrial DNAs in gastric carcinogenesis
2014, Asian Pacific Journal of Cancer Prevention
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Supported by the Seoul Municipal Boramae Hospital (grant 2000-01) affiliated with Seoul National University Hospital. Hee Sung Kim is funded by the BK21 Project for Medicine, Dentistry and Pharmacy.
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Address correspondence and reprint requests to Woo Ho Kim, MD, Department of Pathology, Seoul National University College of Medicine 28 Yongon-dong, Chongno-gu, Seoul 110-799, Korea.