Precursors of gastric carcinoma

E. Strong (ed.). Gastric cancer. Principles and practice. Springer (2015)


The well-defined chronic inflammation-intestinal metaplasia-glandular dysplasia—cancer sequence typically precedes the development of most intestinal type gastric adenocarcinomas [65]. While intestinal metaplasia proceeded by epithelial dysplasia (type I) may be present as a polypoid lesion and resemble a colonic adenoma, it is genetically distinct from the typical tubular adenoma in the colon. In contrast to adenoma-carcinoma sequence in colonic adenocarcinoma (which is usually associated with an intrinsic genetic abnormality in the APC molecular pathway) the progression of intestinal dysplasia to gastric adenocarcinoma occurs with a stepwise accumulation of multiple genetic abnormalities. True de novo gastric adenomas are rare outside the setting of FAP, in which gastric fundic gland polyps progress to epithelial dysplasia secondary to inherent APC gene abnormality. A less common histologic variant of dysplasia is gastric foveolar (type II) dysplasia with a gastric mucin phenotype [66]. The significance of these subtypes remains controversial and phenotyping of gastric dysplasia is not recommended at this time.

The natural history of gastric dysplasia depends on its grade, extent of dysplasia, and surface appearance (polypoid versus flat or depressed). Dysplasia is graded based on cytologic and arhitectural features as either low grade (LGD) or high grade (HGD) (Fig. 4.4a, b). Low-grade dysplasia diagnosed on endoscopic biopsies has been shown to regress in 38–75% of the cases, to persist in 19–50%, and to progress to HGD in 0–9% of the cases [67]. The best independent predictors of progression to adenocarcinoma are lesions greater than 2 cm and a depressed configuration on endoscopic examination [68].

Gastric cancer. Principles and practice (2015) 4.4

Fig. 4.4. Precursors of gastric adenocarcinoma. a) Long standing chronic gastritis is followed by intestinal metaplasia (upper right) and low-grade glandular dysplasia which is demonstrated by nuclear elongation and pseudostratification. b) High-grade dysplasia exhibits loss of cellular polarity of the epithelium with glandular crowding and architectural alteration which approaches the criteria of early carcinoma. c) Even in the absence of invasion into the stroma, early adenocarcinoma proceeded from high-grade dysplasia is demonstrated by expansile crypt growth with cribriform complexity. d) In situ signet ring cell carcinoma is present within the basal membrane with hyperchromatic and depolarized nuclei and pagetoid spread of signet ring cells (arrow)

High-grade dysplasia regresses in only 0–16% of the cases, persists in 14–58%, and progresses in 10–100% to adenocarcinoma (Fig. 4.4c) [67]. Given the high probability of progression to adenocarcinoma, a lesion diagnosed as HGD on endoscopic biopsy should be considered for endoscopic mucosal resection if feasible or surgical resection if HGD is present as multifocal lesions or if endoscopic mucosal resection is not technically feasible.

The precursor of diffuse gastric carcinoma is thought to originate from oxyntic gland tubule neck (or globoid) dysplasia [69] in situ signet ring cell carcinoma. This corresponds to the presence of signet ring cells within the basal membrane, generally with hyperchromatic and depolarized nuclei and pagetoid spread of signet ring cells below the preserved epithelium of glands/ foveolae (Fig. 4.4d) [70].

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