Q-omics provides the consensus-scored SPN profile across patient tissues and cancer cell-line models. SPN 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, SPN is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, SPN protein abundance shows 22,376 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight HNSC, KIRC, and LSCC as cancer lineages where SPN 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 SPN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SPN survival associations across molecular data types. SPN RNA expression shows survival associations in the most cancer types (23), followed by mutation status (8) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SPN RNA expression–survival associations across cancer types. High SPN expression shows unfavorable associations in UVM, but favorable associations in HNSC, UCEC, SKCM, BRCA and CESC. 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 SPN RNA expression.
This table summarizes SPN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for SPN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SPN shows lower tumor expression in LUSC, LUAD and COAD and higher tumor expression in KIRC, KIRP and STAD. The KIRC box plot shows higher SPN RNA expression in tumor versus normal tissue (log2 FC = +2.009, t-test p < 0.001).
This table shows molecular features associated with SPN in patient tissues and cancer cell lines. In patient samples, SPN 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, SPN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in SKIN and UPPER_AERODIGESTIVE_TRACT.
