Q-omics provides the consensus-scored SDS profile across patient tissues and cancer cell-line models. SDS expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, SDS is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, SDS protein abundance shows 22,749 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight ACC, KIRC, and GBM as cancer lineages where SDS 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 SDS — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SDS survival associations across molecular data types. SDS RNA expression shows survival associations in the most cancer types (22), followed by mutation status (6) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SDS RNA expression–survival associations across cancer types. High SDS expression shows unfavorable associations in ACC, UVM, LAML and LUSC, but favorable associations in CESC and KIRC. The ACC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify ACC as the clearest survival context for SDS RNA expression.
This table summarizes SDS 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 9. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for SDS. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SDS shows lower tumor expression in LIHC and higher tumor expression in KIRC, KIRP, HNSC, STAD and LUAD. The KIRC box plot shows higher SDS RNA expression in tumor versus normal tissue (log2 FC = +2.888, t-test p < 0.001).
This table shows molecular features associated with SDS in patient tissues and cancer cell lines. In patient samples, SDS 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, SDS 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 URINARY_TRACT and LARGE_INTESTINE.
