ReviewJournal of translational medicine2026
Decoding the cholangiocarcinoma tumor microenvironment: from single-cell and spatial atlases to translational therapeutic targeting.
Review in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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6 authors.
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Abstract
backgroundCholangiocarcinoma is a heterogeneous biliary malignancy characterized by late diagnosis, stromal desmoplasia, immune exclusion, and frequent resistance to chemotherapy, immunotherapy, and molecularly targeted therapy. Although genomic stratification has enabled biomarker-directed treatment for selected patients, cancer cell-intrinsic alterations alone do not fully explain disease progression or therapeutic failure. MAIN BODY: Recent advances in single-cell RNA sequencing, single-cell multi-omics, spatial transcriptomics, spatial proteomics, multiplex imaging, and pathomics have redefined the CCA tumor microenvironment as an active ecosystem composed of malignant cholangiocytes, cancer-associated fibroblasts, tumor-associated macrophages, regulatory T cells, exhausted CD8 + T cells, natural killer cells, B cells/plasma cells, endothelial cells, extracellular matrix, and tertiary lymphoid structures. These approaches have identified clinically relevant cellular states and spatial niches, including CD146 + vascular cancer-associated fibroblasts, LGALS1 + fibroblasts, SPP1 + macrophages, MEOX1 + regulatory T cells, POSTN+ fibroblast-rich invasive fronts, and CAF-TAM-vascular interaction units. Major communication axes such as IL-6/IL-6R, TGF-β/TGFBR, SPP1/CD44, CXCL12/CXCR4, PD-1/PD-L1, VEGF/VEGFR, and POSTN/integrins connect cellular heterogeneity with immune escape, invasion, angiogenesis, and therapy resistance.
conclusionsThis review synthesizes current single-cell and spatial atlases of CCA and proposes a conceptual translational framework in which TME-derived cellular states, spatial biomarkers, and druggable communication axes may inform patient stratification and rational combination therapy. Because many proposed TME phenotypes and composite biomarkers remain atlas-derived, correlative, or preclinical, this framework should be viewed as a roadmap for prospective validation rather than as a clinically established classification.
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