Figure 4

ADH1B⁺ CAF markers are prognostic for patients with lung adenocarcinoma at early stages. (A) Expression analysis of the top 25 differentially expressed genes related to the ADH1B+ CAF cluster across all CAF clusters. (B) Gene expression of ADH1B⁺ CAF markers across all identified subpopulations of cells. (C) Representative images of MxIF staining showing expression of PanCK and ADH1B in LUAD tissue isolated from patients with predicted indolent and aggressive tumor behavior. Corresponding cellular density of ADH1B⁺ CAFs (cell/mm²) in the LUAD tissue extracted from the patients with predicted indolent or aggressive tumor behavior (indolent n = 7, aggressive n = 6, *—p < 0.05, data showed as mean ± SEM). (D) Cell enrichment analysis (CIBERSORT) of LUAD patient samples (stage I and II, TCGA dataset). Violin plots demonstrate ADH1B⁺ CAF enrichment scores in TCGA samples with low (n = 105), intermediate (n = 209), and high (n = 105) expression of ADH1B (*p < 0.05). (E) Gene expression level of ADH1B in LUAD samples (TCGA dataset) at different stages of development (independent samples, stage I n = 294, stage II n = 125, stage III n = 84, stage IV n = 26, *p < 0.05). (F) Kaplan–Meier analysis of the overall survival of LUAD patients with low (n = 105), intermediate (n = 209), and high (n = 105) expression of ADH1B (stage I and II, TCGA dataset). (G) Kaplan–Meier analysis (KM-plotter data) of the overall survival of patients with LUADs at stage I and characterized by low and high expression of top marker genes associated with ADH1B⁺ CAF subpopulation (ADH1B (low n = 185, high n = 185), CFD (low n = 288, high n = 289), SEPP1 ((low n = 288, high n = 289)), DCN (low n = 288, high n = 289), and A2M (low n = 288, high n = 289).