Q-omics provides the consensus-scored CCK profile across patient tissues and cancer cell-line models. CCK expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, CCK is differentially expressed in 8, with the highest sampling consensus in KIRC. Additionally, CCK RNA expression shows 14,058 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight LUAD, KIRC, and GBM as cancer lineages where CCK 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 CCK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CCK survival associations across molecular data types. CCK RNA expression shows survival associations in the most cancer types (24), followed by mutation status (1) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CCK RNA expression–survival associations across cancer types. High CCK expression shows unfavorable associations in LUAD, KIRP, LUSC, OV and UVM, but favorable associations in KIRC. The LUAD 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 LUAD as the clearest survival context for CCK RNA expression.
This table summarizes CCK tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CCK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CCK shows lower tumor expression in KIRC, THCA, LUAD, LUSC and KICH and higher tumor expression in PAAD. The KIRC box plot shows higher CCK RNA expression in normal versus tumor tissue (log2 FC = −0.107, t-test p < 0.001).
This table shows molecular features associated with CCK in patient tissues and cancer cell lines. In patient samples, CCK 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, CCK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in BONE and CNS.
