Q-omics provides the consensus-scored FCN3 profile across patient tissues and cancer cell-line models. FCN3 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, FCN3 is differentially expressed in 15, with the highest sampling consensus in LUAD. Additionally, FCN3 protein abundance shows 20,106 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, LUAD, and LSCC as cancer lineages where FCN3 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 FCN3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FCN3 survival associations across molecular data types. FCN3 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (3) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FCN3 RNA expression–survival associations across cancer types. High FCN3 expression shows unfavorable associations in LUSC, but favorable associations in KIRC, SKCM, HNSC, THCA and LIHC. 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 FCN3 RNA expression.
This table summarizes FCN3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 7. The strongest signals are observed in LUAD for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for FCN3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FCN3 shows lower tumor expression in LUAD, KIRP, LIHC and LUSC and higher tumor expression in COAD and HNSC. The LUAD box plot shows higher FCN3 RNA expression in normal versus tumor tissue (log2 FC = −5.338, t-test p < 0.001).
This table shows molecular features associated with FCN3 in patient tissues and cancer cell lines. In patient samples, FCN3 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, FCN3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and SOFT_TISSUE.
