Q-omics provides the consensus-scored C1R profile across patient tissues and cancer cell-line models. C1R expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, C1R is differentially expressed in 12, with the highest sampling consensus in KICH. Additionally, C1R protein abundance shows 29,607 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRC, KICH, and PDAC as cancer lineages where C1R 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 C1R — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes C1R survival associations across molecular data types. C1R RNA expression shows survival associations in the most cancer types (24), followed by mutation status (9) 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 C1R RNA expression–survival associations across cancer types. High C1R expression shows unfavorable associations in KIRC, UVM and LGG, but favorable associations in SKCM, LIHC and MESO. 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 C1R RNA expression.
This table summarizes C1R tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, 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 C1R. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. C1R shows lower tumor expression in KICH, THCA, BLCA and LIHC and higher tumor expression in HNSC and KIRC. The KICH box plot shows higher C1R RNA expression in normal versus tumor tissue (log2 FC = −4.128, t-test p < 0.001).
This table shows molecular features associated with C1R in patient tissues and cancer cell lines. In patient samples, C1R 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, C1R RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and LARGE_INTESTINE.
