Q-omics provides the consensus-scored CCKAR profile across patient tissues and cancer cell-line models. CCKAR expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in BRCA. Among the 18 cancer types available for tumor–normal comparison, CCKAR is differentially expressed in 8, with the highest sampling consensus in KIRC. Additionally, CCKAR RNA expression shows 13,325 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight BRCA, KIRC, and THYM as cancer lineages where CCKAR 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 CCKAR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CCKAR survival associations across molecular data types. CCKAR RNA expression shows survival associations in the most cancer types (19), followed by mutation status (6) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CCKAR RNA expression–survival associations across cancer types. High CCKAR expression shows unfavorable associations in LGG, KIRC, UVM and ACC, but favorable associations in BRCA and HNSC. The BRCA Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .006). Together, the overview and detailed table identify BRCA as the clearest survival context for CCKAR RNA expression.
This table summarizes CCKAR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for CCKAR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CCKAR shows lower tumor expression in KIRC, STAD and KIRP and higher tumor expression in BRCA, KICH and PRAD. The KIRC box plot shows higher CCKAR RNA expression in normal versus tumor tissue (log2 FC = −0.215, t-test p < 0.001).
This table shows molecular features associated with CCKAR in patient tissues and cancer cell lines. In patient samples, CCKAR shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, CCKAR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BLOOD_Leukemia.
