Q-omics provides the consensus-scored FMN2 profile across patient tissues and cancer cell-line models. FMN2 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, FMN2 is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, FMN2 RNA expression shows 16,317 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KIRP, KIRC, and TGCT as cancer lineages where FMN2 shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for FMN2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FMN2 survival associations across molecular data types. FMN2 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (13) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FMN2 RNA expression–survival associations across cancer types. High FMN2 expression shows unfavorable associations in KIRP, BLCA, MESO, THCA, UVM and KIRC. The KIRP Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRP as the clearest survival context for FMN2 RNA expression.
This table summarizes FMN2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for FMN2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FMN2 shows lower tumor expression in KIRC, COAD, KIRP, THCA, BRCA and READ. The KIRC box plot shows higher FMN2 RNA expression in normal versus tumor tissue (log2 FC = −1.188, t-test p < 0.001).
This table shows molecular features associated with FMN2 in patient tissues and cancer cell lines. In patient samples, FMN2 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, FMN2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BONE.
