Fibroblasts were extracted from samples of EOC to use as a primary source. For this purpose, researchers obtained expression profiles from microdissection and single-cell RNA sequencing (scRNA-seq) datasets (such as TCGA, GSE9891, GSE63885, GSE118828, and GSE178913). To investigate the link between FMO2 and stromal activation and immunological infiltration, they performed a gene set enrichment analysis (GSEA). Independent EOC cohort (n = 113) confirmed the prognostic significance of FMO2 and combined macrophage infiltration level. 

They found that FMO2 expression was augmented in tumor stroma and that this increase was linked to fibroblast activation. In addition, FMO2 was able to predict a poorer clinical outcome for patients with EOC. FMO2 was found to promote the recruitment of tumor-infiltrating lymphocytes in the mesenchymal subtype of EOC, as evidenced by the signature defined by FMO2. In addition, they demonstrated that the expression of FMO2 in conjunction with CD163+ cell infiltration level in the tumor stroma could predict poor overall survival (HR = 3.63, 95% CI = 1.93-6.84, P = 0.0008) in patients with EOC. 

In addition, FMO2’s ability to utilize the expression of immunological checkpoints to forecast the prognosis of patients with ovarian cancer was also demonstrated (such as PD-L1 and PD1). These findings discuss the significance of FMO2 in supporting tumor growth in EOC and its relationship with immunological components, suggesting that it may be a promising target for stroma-oriented treatments against EOC.