ArticleFrontiers in oncology2026
RTK-RAS pathway alterations in hepatocellular carcinoma and cholangiocarcinoma: a multicohort genomic and single-cell transcriptomic study.
Article in Frontiers in oncology, 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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Abstract
Objective: To determine whether heterogeneous genomic alterations detected by clinical tumor panels converge on a reproducible pathway-level difference between hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), and to examine its transcriptional output, cellular localization, and tumor-stromal coexpression context in public multi-omics cohorts. Methods: The institutional cohort comprised 52 patients who underwent tumor tissue genomic testing, including 28 with HCC and 24 in a CCA working cohort whose intrahepatic location was not uniformly documented. Ten canonical oncogenic pathways were compared using panel-aware evaluable denominators, and the selected pathway was tested in independent Memorial Sloan Kettering (MSK) cohorts. Matched genomic and transcriptomic data from The Cancer Genome Atlas (TCGA) were used to evaluate downstream pathway activity. GSE151530 and GSE189903 were analyzed by patient-level pseudobulk to localize the transcriptional difference, followed by CellChatDB-guided ligand-receptor coexpression analysis. Results: Receptor tyrosine kinase-RAS (RTK-RAS) showed the strongest cancer-type difference in the institutional cohort: alterations were detected in 4/21 evaluable HCC cases and 8/11 evaluable CCA cases (odds ratio [OR] = 9.44; 95% CI, 1.87-47.70; P = 0.00601; Benjamini-Hochberg-adjusted q = 0.0601), with concordant directions across sensitivity analyses. In MSK, integrated RTK-RAS alterations occurred in 240/412 intrahepatic cholangiocarcinoma (iCCA) cases (58.3%) and 107/289 HCC cases (37.0%; OR = 2.37; 95% CI, 1.74-3.22; P = 3.12 × 10 Conclusion: Panel-aware integration of clinical genomic testing and public multi-omics data supports a higher burden of heterogeneous RTK-RAS alterations in CCA/iCCA than in HCC and links this difference to a malignant-cell MAPK transcriptional phenotype. The pathway-level framework complements, rather than replaces, established alteration-specific interpretation and generates tumor-stromal coexpression hypotheses for further spatial and functional testing.
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