Dysplasia, Neoplasia, and Adenoma
In modern gastrointestinal pathology, the terms dysplasia and neoplasia ("formation of new tissue") are entirely equivalent. The combined term "dysplasia/neoplasia" is frequently used. The process begins when an epithelial cell accumulates somatic mutations. This triggers clonal proliferation, forming a clone of cells with autonomous growth.
The key morphological feature of these changes is that they are phenotypically identical to tumor growth, yet strictly restricted to the basement membrane. The cells lose normal differentiation, and tissue histoarchitecture is disrupted.
In the context of non-invasive neoplasia, this concept is also equivalent to an adenoma (which is likewise divided into low and high grades). This classification is actively used not only for the stomach but also for evaluating mucosal changes in ulcerative colitis or Barrett esophagus. The clinical significance of these conditions is immense: they obligately progress to invasive carcinoma, and precise staging is critical for determining treatment strategy and the scope of surgical resection.
WHO Grades of Intraepithelial Neoplasia
Intraepithelial neoplasia serves as a direct precursor to progression into invasive growth and subsequent metastasis. The WHO classification divides it into two categories:
- Low-grade neoplasia. Corresponds to mild and moderate dysplasia. Morphologically, numerous small, round glandular structures are identified. Cells elongate and completely lose their ability to produce mucus. Nuclei acquire an elongated, cigar-like shape of varying sizes and are predominantly located basally. Nucleoli are rare. Slight pseudostratification (nuclei lying at different levels) may occur. An important criterion for differential diagnosis: cells with elongated nuclei are located specifically in the superficial compartments of the mucosa. This distinguishes true neoplasia from "indefinite for neoplasia"—repair-related changes capable of regression.
- High-grade neoplasia. Equivalent to severe dysplasia and carcinoma in situ (in stratified squamous epithelium). Sometimes designated as high-grade intraglandular neoplasia. Characterized by a sharp increase in nuclear and cellular atypia. Mucus production is completely absent. Cells closely abut the basement membrane. Nuclei become large, round, or cigar-shaped, with a coarse nuclear membrane of uneven thickness. Marked nuclear stratification is observed, and nucleoli are ubiquitous.
Intestinal Metaplasia as a Background for Tumor Growth
Gastric mucosa alterations are frequently accompanied by the appearance of cells characteristic of the intestine. Two types of metaplasia are distinguished:
- Complete metaplasia (small intestinal, type I). The cellular composition of the mucosa becomes maximally similar to the small intestine. Properly structured mucus-producing goblet cells and absorptive enterocytes with a brush border appear. Paneth cells and endocrine cells are encountered less frequently. To date, the exact clinical and prognostic significance of this phenomenon remains undetermined.
- Incomplete metaplasia (colonic, type II). Characterized by the appearance of goblet cells containing mucus vacuoles of markedly varying sizes. This mucus represents a mixture of sialomucins and sulfomucins. On routine hematoxylin and eosin staining, mucus-engorged mucocytes can closely resemble goblet cells, making special stains essential for precise identification.
Foci of complete and incomplete metaplasia can coexist in a single biopsy specimen. However, it is critically important to remember that incomplete intestinal metaplasia is most frequently found adjacent to areas of epithelial dysplasia and early gastric cancer.