Q-omics provides the consensus-scored SCN4A profile across patient tissues and cancer cell-line models. SCN4A expression is associated with patient survival in 31 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, SCN4A is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, SCN4A protein abundance shows 22,121 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRC, and PDAC as cancer lineages where SCN4A 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 SCN4A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SCN4A survival associations across molecular data types. SCN4A RNA expression shows survival associations in the most cancer types (31), followed by mutation status (9) 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 SCN4A RNA expression–survival associations across cancer types. High SCN4A expression shows unfavorable associations in UVM, UCEC and COAD, but favorable associations in KIRC, LUAD 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 SCN4A RNA expression.
This table summarizes SCN4A 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 5. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for SCN4A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SCN4A shows lower tumor expression in KIRP, HNSC, BRCA and KICH and higher tumor expression in KIRC and LIHC. The KIRC box plot shows higher SCN4A RNA expression in tumor versus normal tissue (log2 FC = +1.190, t-test p < 0.001).
This table shows molecular features associated with SCN4A in patient tissues and cancer cell lines. In patient samples, SCN4A 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, SCN4A 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 UPPER_AERODIGESTIVE_TRACT and LARGE_INTESTINE.