ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2026
EML4-ALK fusion rewires transcriptomic, miRNA, and CAF-associated programs in non-small cell lung cancer.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 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
purposeThis study presents an integrative analysis of paired mRNA/miRNA expression and tumor microenvironment features to characterize the molecular landscape associated with EML4-ALK fusion status in non-small cell lung cancer (NSCLC).
methodsUsing TCGA-derived fusion-positive and fusion-negative NSCLC cohorts, we compared three complementary layers of tumor biology: transcriptomic architecture, miRNA-mRNA regulatory networks, and immune-stromal composition.
resultsFusion-positive tumors exhibited a distinct molecular program characterized by metabolic and proteostasis reprogramming, including glycolytic and N-glycan biosynthetic pathways linked to endoplasmic reticulum protein processing and export. Relative to fusion-negative tumors, they also showed reduced stromal infiltration and attenuation of extracellular matrix, adhesion, calcium signaling, and cytokine-related transcriptional programs. Integrative miRNA analysis identified a fusion-associated, miR-3065-centered regulatory hub with predicted extracellular matrix- and adhesion-related targets,including PDGFRB, CTSK, COL4A2, SPARC, FBN1, and LUM, whereas fusion-negative tumorsshowed miRNA network alterations associated with proliferative and ciliary programs. Tumormicroenvironment analysis further distinguished the groups, with fusion-positive tumors showing reduced cancer-associated fibroblast infiltration.
conclusionThese findings characterize distinct molecular and microenvironmental features associated with EML4-ALK fusion-positive NSCLC and identify candidate regulatory networks and biomarkers that, pendingvalidation, may inform subtype-specific therapeutic stratification.
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