Q-omics provides the consensus-scored FCN1 profile across patient tissues and cancer cell-line models. FCN1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, FCN1 is differentially expressed in 11, with the highest sampling consensus in LUAD. Additionally, FCN1 protein abundance shows 25,471 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight HNSC, LUAD, and GBM as cancer lineages where FCN1 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 FCN1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FCN1 survival associations across molecular data types. FCN1 RNA expression shows survival associations in the most cancer types (23), 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 FCN1 RNA expression–survival associations across cancer types. High FCN1 expression shows unfavorable associations in KIRP and LUSC, but favorable associations in HNSC, SKCM, LUAD and PAAD. 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 FCN1 RNA expression.
This table summarizes FCN1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for FCN1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FCN1 shows lower tumor expression in LUAD, LUSC, KICH, BLCA and BRCA and higher tumor expression in KIRC. The LUAD box plot shows higher FCN1 RNA expression in normal versus tumor tissue (log2 FC = −1.838, t-test p < 0.001).
This table shows molecular features associated with FCN1 in patient tissues and cancer cell lines. In patient samples, FCN1 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, FCN1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BLOOD_Leukemia.
