Q-omics provides the consensus-scored CKB profile across patient tissues and cancer cell-line models. CKB expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, CKB is differentially expressed in 16, with the highest sampling consensus in BLCA. Additionally, CKB protein abundance shows 18,554 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, BLCA, and GBM as cancer lineages where CKB 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 CKB — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CKB survival associations across molecular data types. CKB RNA expression shows survival associations in the most cancer types (21), followed by 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 CKB RNA expression–survival associations across cancer types. High CKB expression shows unfavorable associations in THCA, but favorable associations in KIRP, SCLC, KIRC, CESC and SARC. The KIRP Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRP as the clearest survival context for CKB RNA expression.
This table summarizes CKB tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 6. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CKB. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CKB shows lower tumor expression in BLCA, STAD, KIRC, THCA and COAD and higher tumor expression in LIHC. The BLCA box plot shows higher CKB RNA expression in normal versus tumor tissue (log2 FC = −5.325, t-test p < 0.001).
This table shows molecular features associated with CKB in patient tissues and cancer cell lines. In patient samples, CKB 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, CKB 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 CNS and BLOOD_Leukemia.
