Send to

Choose Destination
Am J Surg Pathol. 1989 Aug;13(8):685-90.

Histological classification of intraepithelial neoplasias and microinvasive squamous carcinoma of the esophagus.

Author information

Department of Pathology, Chinese Academy of Medical Sciences, Beijing.


We reviewed a total of 119 resected esophagi with intraepithelial neoplasias of low grade (including slight or moderate dysplasias), high grade (including severe dysplasia and carcinoma in situ), or microinvasive squamous carcinoma (i.e., not invasive beyond the submucosa and without metastases in regional lymph nodes). Epithelial buds bulging into the stroma were noted in noninvasive intraepithelial lesions. The most severe degree of histological alteration was used to characterize each case. Of the 119 cases, five were low-grade, 38 were high-grade, and the remaining 76 specimens contained microinvasive squamous carcinoma. Of these, 23 invaded only the lamina propria. Nine invaded the muscularis mucosae, 16 invaded the inner half of the submucosa, and the remaining 28 invaded the outer half of the submucosa. Epithelial buds were divided according to their configuration into types I, II, and III. Grade I was characterized by regular epithelial buds of the same size, grade II had regular buds that varied in size, and grade III had irregular buds (i.e., buds of varying length and width with irregular contours). Our study of 66 specimens with microinvasive squamous carcinoma showed that one of the two specimens that had low grade dysplasia also had type III buds, while 56 of the remaining 64 (87.7%) with high grade dysplasia also had type III buds. Microinvasion originated at the tip of the type III epithelial buds in 12 specimens. Similar results have been demonstrated in experimental animals. We conclude that in the esophageal mucosa, there is a close relationship among the degree of squamous cellular atypia, the formation of epithelial buds, and the progression toward invasive carcinoma.

[Indexed for MEDLINE]

Supplemental Content

Loading ...
Support Center