Q-omics provides the consensus-scored FMOD profile across patient tissues and cancer cell-line models. FMOD expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, FMOD is differentially expressed in 13, with the highest sampling consensus in THCA. Additionally, FMOD protein abundance shows 25,666 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight HNSC, THCA, and PDAC as cancer lineages where FMOD 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 FMOD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FMOD survival associations across molecular data types. FMOD RNA expression shows survival associations in the most cancer types (27), followed by mutation status (6) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FMOD RNA expression–survival associations across cancer types. High FMOD expression shows unfavorable associations in LGG, BLCA, THCA and ACC, but favorable associations in HNSC and UVM. The HNSC 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 HNSC as the clearest survival context for FMOD RNA expression.
This table summarizes FMOD 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 6. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for FMOD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FMOD shows lower tumor expression in THCA, KICH, UCEC, BRCA and KIRC and higher tumor expression in HNSC. The THCA box plot shows higher FMOD RNA expression in normal versus tumor tissue (log2 FC = −2.625, t-test p < 0.001).
This table shows molecular features associated with FMOD in patient tissues and cancer cell lines. In patient samples, FMOD shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, FMOD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and BREAST.
