Q-omics provides the consensus-scored FMO1 profile across patient tissues and cancer cell-line models. FMO1 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, FMO1 is differentially expressed in 13, with the highest sampling consensus in THCA. Additionally, FMO1 protein abundance shows 21,306 significant protein co-abundance associations, with the highest sampling consensus in CCRCC. Together, these results highlight KIRC, THCA, and CCRCC as cancer lineages where FMO1 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 FMO1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FMO1 survival associations across molecular data types. FMO1 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (8) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FMO1 RNA expression–survival associations across cancer types. High FMO1 expression shows unfavorable associations in LIHC, ACC and LGG, but favorable associations in KIRC, DLBC and ESCA. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for FMO1 RNA expression.
This table summarizes FMO1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 7. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for FMO1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FMO1 shows lower tumor expression in THCA, KICH, HNSC and UCEC and higher tumor expression in LUAD and LUSC. The THCA box plot shows higher FMO1 RNA expression in normal versus tumor tissue (log2 FC = −1.006, t-test p < 0.001).
This table shows molecular features associated with FMO1 in patient tissues and cancer cell lines. In patient samples, FMO1 shows the broadest associations at the RNA and protein expression levels, with CCRCC recurring as the lineage with the largest associated feature set. In cancer cell lines, FMO1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BLOOD_Lymphoma.
