Gastric-type well-differentiated adenocarcinoma and pyloric gland adenoma of the stomach

Abstract

found that gastric carcinomas could be broadly divided into gland-forming adenocarcinomas and poorly differentiated carcinomas, which included signet-ring cell carcinomas. The former were found to retain intestinal features, and the latter tended to disclose a diffusely infiltrative growth pattern; Laurén referred to these as intestinal-type and diffuse-type, respectively, reporting that 53% of his samples were intestinal-type, 33% were diffuse-type, and the remaining 14% were unclassifiable [1].In the differentiated adenocarcinomas, intestinal metaplasia was often seen in the stomach, and intestinaltype cancers were thought to arise from the intestinal metaplasia. On the other hand, diffuse-type cancers did not retain intestinal characteristics, and they were considered to arise in the ordinary gastric mucosa, which was not involved in intestinal metaplasia [2,3]. In the middle of the 1980s, Helicobacter pylori was found to cause chronic active gastritis, and it was suggested that H. pylori played an important role in gastric carcinogenesis. In this respect, a hypothesis was that H. pylori caused chronic active gastritis with intestinal metaplasia, resulting in the development of intestinal-type adenocarcinomas [4,5].However, several studies appeared which described well-differentiated adenocarcinomas arising in nonintestinalized gastric mucosa, and there has been a question whether well-differentiated adenocarcinomas of the stomach were exclusively intestinal type. The recent discovery of MUC genes coding core proteins of mucin has identified the phenotypic expression of gastrointestinal neoplasms [6][7][8]. The disease entity of "gastric-type well-differentiated adenocarcinoma" has recently been accepted, especially in Japan and Europe. This entity has often been a clinicopathological subject of discussion, especially in Japanese journals, because its biological behavior is possibly highly malignant, in spite of the difficulty of making endoscopic and histopathological diagnoses [9,10]. AbstractSince 1985, when gastric-type well-differentiated adenocarcinomas were demonstrated in hyperplastic polyps of the stomach, we have studied phenotypic expression in gastrointestinal epithelial lesions. The recent discovery of MUC genes coding core proteins of mucin has improved research on the phenotypic expression of gastrointestinal neoplasms. The disease entity of gastric-type well-differentiated adenocarcinoma has recently been accepted, especially in Japan and Europe. This entity has often become a clinicopathological subject of discussion, because its biological behavior is possibly highly malignant, in spite of the difficulty in making endoscopic and histopathological diagnoses. Even under these circumstances, the term "gastric adenoma" usually means flat adenoma of the intestinal type. Gastric-type adenomas have been regarded as exceptional until recently. Although gastric-type adenomas could theoretically be classified into foveolar type and pyloric-gland type, foveolar-type adenoma is, in practice, difficult t...

“Crawling-type” adenocarcinoma of the stomach: a distinct entity preceding poorly differentiated adenocarcinoma

“…The implications for the diagnosis of CTAC have been described previously in several Japanese reports and review articles [10][11][12][13]. To our knowledge, however, there are no systematic studies of CTAC in which surgically or endoscopically resected specimens have been used.…”

“…In a review article by Kushima et al [13] adenocarcinoma with characteristic glandular structures, called ''shaking-hands structures'', which seems essentially identical to CTAC, was regarded as a ''prediffuse type''. Our hypothesis may support their concept.…”

“…Occasionally, signet-ring cells are found. Although the importance of recognizing this subgroup has been mentioned in other review articles [12,13], the clinicopathological characteristics of CTAC have not been adequately described.…”

Epithelial dysplasia of the stomach with gastric immunophenotype shows features of biological aggressiveness

“…However, evidence from the literature points to the possible existence of alternative pathways in which intestinal metaplasia may not be involved. Evidence stems mainly from the study of tiny early GCs arising in nonmetaplastic mucosa, as described by Japanese authors [14,15] as well as the studies of the expression of markers of gastric differentiation in dysplasia and gastric adenocarcinoma [7, 10, 16, 17]. The latter demonstrate that both types of lesions may express, predominantly or exclusively, markers of gastric differentiation, raising the possibility of an origin in native gastric mucosa, rather than in intestinal metaplastic lesions.…”

Practical Points in Gastric Pathology

“…24 Sporadic PGAs show some chromosomal abnormalities, including 17pq and 20q gains and 4q, 5q, and 6q losses 24 along with frequent GNAS (48%, 11 of 23) and KRAS (41%, 9 of 23) mutations. 25 On the other hand, Lynch syndromeassociated PGAs have been shown to be affected by mutations in various DNA mismatch repair genes, resulting in mismatch repair protein expressions.…”