Major Histological Types and Development
Pathology divides gastric cancer into two fundamentally different variants:
- Intestinal-type carcinoma: Develops step-by-step through precancerous states. The classic Correa cascade involves H. pylori colonization, chronic gastritis, gastric atrophy, intestinal metaplasia, dysplasia (adenoma), and progression to invasive carcinoma. Mutations in APC, p53, K-ras, and DNA methylation changes are commonly identified at these stages.
- Diffuse-type carcinoma: Arises de novo, bypassing metaplasia and adenoma stages. It is characterized by genetic instability, p53 mutations, loss or mutation of the E-cadherin gene (CDH1), and the formation of signet-ring cell structures rich in mucin.
The extreme manifestation of diffuse endophytic growth is linitis plastica (linitis plastica), which causes marked, rigid thickening of the gastric wall.
Borrmann Macroscopic Classification
To describe advanced gross forms of the tumor, the Borrmann classification divides the process into four types:
- Type 1 (Polypoid / Fungating) — Exophytic solitary mass forming a nodule or cauliflower-like lesion with clear borders from healthy tissue.
- Type 2 (Ulcerated with distinct margins) — Crater-like "ulcer-cancer" with elevated, rolled borders and clear demarcation from the mucosa.
- Type 3 (Ulcerofungating / Infiltrative) — Ulceration without clear boundaries, sloping edges, and deep invasion into the wall layers.
- Type 4 (Diffusely infiltrative / Linitis plastica) — Endophytic growth with diffuse wall thickening and loss of fold pliability.
Early Gastric Cancer and Precancerous Changes
The term early gastric cancer refers to a tumor restricted to the mucosa or submucosa, critically sparing the muscularis propria of the organ wall. Despite this limitation, the presence of lymphatic channels in the lamina propria means a baseline risk of lymph node metastasis still exists.
The central concept of gastrointestinal precancerous lesions is intraepithelial neoplasia (epithelial dysplasia):
- Adenoma is considered an obligate precancerous lesion with a high risk of malignant transformation.
- Atrophic gastritis increases the risk of malignant transformation several-fold.
- Reactive foveolar hyperplasia (a response to H. pylori or NSAIDs) is not considered a premalignant change.