Q-omics provides the consensus-scored C1S profile across patient tissues and cancer cell-line models. C1S expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, C1S is differentially expressed in 14, with the highest sampling consensus in KICH. Additionally, C1S protein abundance shows 27,689 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRC, KICH, and PDAC as cancer lineages where C1S 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 C1S — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes C1S survival associations across molecular data types. C1S RNA expression shows survival associations in the most cancer types (22), followed by mutation status (7) 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 C1S RNA expression–survival associations across cancer types. High C1S expression shows unfavorable associations in KIRC, KIRP, LGG and UVM, but favorable associations in LIHC and SKCM. The KIRC 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 KIRC as the clearest survival context for C1S RNA expression.
This table summarizes C1S tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 5. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for C1S. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. C1S shows lower tumor expression in KICH, THCA, BLCA and LIHC and higher tumor expression in HNSC and KIRC. The KICH box plot shows higher C1S RNA expression in normal versus tumor tissue (log2 FC = −4.215, t-test p < 0.001).
This table shows molecular features associated with C1S in patient tissues and cancer cell lines. In patient samples, C1S 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, C1S RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in OESOPHAGUS and BONE.
