## Intestinal vs. Diffuse-Type Gastric Adenocarcinoma ### Histopathological Distinction **Key Point:** The Lauren classification divides gastric carcinoma into intestinal and diffuse types based on growth pattern and cellular morphology — the most reliable discriminator is the presence or absence of glandular differentiation. ### Comparison Table | Feature | Intestinal Type | Diffuse Type | | --- | --- | --- | | **Growth pattern** | Forms well-organized glands and tubules | Infiltrative, scattered cells | | **Cell morphology** | Columnar cells, mucin-secreting | Signet-ring cells (often) | | **Background mucosa** | Intestinal metaplasia, atrophy | Normal or minimally altered | | **Cohesion** | Cells maintain adhesion | Loss of E-cadherin, poor adhesion | | **Prognosis** | Generally better | Generally worse | | **Associated risk factors** | H. pylori, diet, smoking | Genetic predisposition (CDH1 mutations) | ### Key Distinguishing Feature **High-Yield:** Intestinal-type carcinomas show **well-formed glandular/tubular structures** with evidence of intestinal differentiation (intestinal metaplasia in background mucosa). This is the pathognomonic finding that separates it from diffuse type. **Clinical Pearl:** Diffuse-type carcinomas (especially signet-ring cell variant) lack glandular organization and show individual cell infiltration — they often present at advanced stage because they are not detected early and spread submucosally without forming a discrete mass. ### Pathogenesis Context - **Intestinal type:** Arises through Correa cascade (normal → chronic gastritis → atrophy → intestinal metaplasia → dysplasia → carcinoma). H. pylori is a major driver. - **Diffuse type:** Often associated with hereditary diffuse gastric cancer (HDGC) syndrome due to CDH1 (E-cadherin) mutations; may occur without preceding intestinal metaplasia. **Mnemonic:** **GLAND** = Glandular structures = Intestinal type; **SCATTER** = Scattered signet-ring cells = Diffuse type.
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