title: Malignant transformation of gastric hyperplastic polyps: alteration of phenotypes, proliferative activity, and p53 expression.
abstract: The aim of this study was to clarify the mechanism of malignant transformation of gastric hyperplastic polyps, focusing on phenotypic expression, cell proliferation, and p53 overexpression. Twenty-two lesions of gastric hyperplastic polyps with neoplastic foci were selected for this study. The phenotypes were divided into 3 types (G, gastric; incomp I, incomplete intestinal; and comp I, complete intestinal), according to immunohistochemical stains (human gastric mucin [HGM], MUC2, and CD10). The cell proliferative activity by Ki-67 and overexpression of p53 protein were also examined. Eleven of these lesions contained carcinoma components (CA, category 5 by the Vienna classification), 6 of which were accompanied by low-grade dysplasia (LGD, category 3) and 4 of which were accompanied by high-grade dysplasia (HGD, category 4). Another 2 were composed only of HGD, and the remaining 9 were composed of both LGD and HGD components. As a result, 15 LGD, 15 HGD, and 11 CA components were recognized. The 15 LGD components were classified as 1 G type and 14 incomp I type. All hyperplastic components expressed HGM, 5 (22.7%) of which were accompanied by focal intestinal metaplasia demonstrated by MUC2 expression, whereas intestinalization frequently occurred in neoplastic components (93% of LGD, 53% of HGD, and 64% of CA components). The labeling index was 22.2% in hyperplastic, 42.2% in LGD, 55.7% in HGD, and 53.9% in CA components. p53 protein overexpression was recognized in none of hyperplastic, in 40% of the LGD, in 60% of the HGD, and in 45% of the CA components. These results suggest the importance of the dysplasia-carcinoma sequence in malignant transformation of hyperplastic polyps. Interestingly, intestinalization frequently occurs during neoplastic transformation, although it is not common in the surrounding hyperplastic components.
authors.affiliation: Department of Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Yao
authors.forename: Masaaki
authors.initials: M
authors.lastname: Kajiwara
authors.forename: Sigekazu
authors.initials: S
authors.lastname: Kuroiwa
authors.forename: Akinori
authors.initials: A
authors.lastname: Iwashita
authors.forename: Masafumi
authors.initials: M
authors.lastname: Oya
authors.forename: Akira
authors.initials: A
authors.lastname: Kabashima
authors.forename: Masazumi
authors.initials: M
authors.lastname: Tsuneyoshi
mesh_terms: D000951:Antigens, Neoplasm / Q000032:analysis; D002455:Cell Division; D002471:Cell Transformation, Neoplastic; D006801:Humans; D007150:Immunohistochemistry; D011127:Polyps / Q000378:metabolism / Q000473:pathology*; D013274:Stomach Neoplasms / Q000378:metabolism / Q000473:pathology*; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis*
chemical_list: D000951:Antigens, Neoplasm; D016159:Tumor Suppressor Protein p53