Q-omics provides the consensus-scored C1RL profile across patient tissues and cancer cell-line models. C1RL 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, C1RL is differentially expressed in 10, with the highest sampling consensus in KIRP. Additionally, C1RL protein abundance shows 25,070 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRC, KIRP, and PDAC as cancer lineages where C1RL 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 C1RL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes C1RL survival associations across molecular data types. C1RL RNA expression shows survival associations in the most cancer types (24), followed by mutation status (4) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible C1RL RNA expression–survival associations across cancer types. High C1RL expression shows unfavorable associations in KIRC and LGG, but favorable associations in SKCM, HNSC, MESO and BRCA. 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 C1RL RNA expression.
This table summarizes C1RL 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 8. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for C1RL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. C1RL shows lower tumor expression in KICH, LIHC and BRCA and higher tumor expression in KIRP, KIRC and HNSC. The KIRP box plot shows higher C1RL RNA expression in tumor versus normal tissue (log2 FC = +1.590, t-test p < 0.001).
This table shows molecular features associated with C1RL in patient tissues and cancer cell lines. In patient samples, C1RL 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, C1RL 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 OESOPHAGUS and BLOOD_Lymphoma.
