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Life sciences · Journal article
Frontiers in Pharmacology · October 22, 2026
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Colorectal mucinous adenocarcinoma (CMA) is a histologically and molecularly distinct subtype of colorectal cancer (CRC), marked by abundant extracellular mucin, a predilection for the proximal colon, and frequent overlap with deficient mismatch repair/high microsatellite instability (dMMR/MSI-H), BRAF V600E mutation, CpG island methylator phenotype-high (CIMP-high) status, and serrated pathway biology. Although immune checkpoint inhibitors and molecularly targeted therapies have expanded treatment options for selected patients with advanced CRC, treatment strategies tailored to the histologic phenotype, lineage programs, and microenvironmental architecture of CMA remain limited. CLDN18.2, the gastric isoform encoded by CLDN18, is now a clinically validated therapeutic target in gastric and gastroesophageal junction (GEJ) adenocarcinomas. Recent pathology-based studies suggest that CLDN18.2 expression is uncommon in unselected conventional colorectal adenocarcinoma but enriched in CMA, mucin-rich CRC, and tumors with gastric-type or foregut-like differentiation, particularly those arising in the proximal colon or harboring dMMR/MSI-H status or BRAF V600E mutation. This pattern suggests that CLDN18.2 in CMA is unlikely to be a classic oncogenic driver; instead, it is better viewed as a therapeutically accessible, lineage-associated membrane antigen. This review summarizes the biological rationale, expression data, companion diagnostic issues, therapeutic platforms, and translational barriers relevant to CLDN18.2 in CMA. We propose a framework centered on lineage reprogramming, antigen enrichment, assay standardization, and therapeutic translation. Current evidence supports CLDN18.2 as a candidate biomarker for biomarker-enriched investigation, not as an established therapeutic target in CMA. Future work should prioritize CMA-specific preclinical models, standardized membranous immunohistochemistry (IHC) scoring, and prospective trials that integrate CLDN18.2 expression with molecular subtype and tumor microenvironmental features.