Q-omics provides the consensus-scored CKS1B profile across patient tissues and cancer cell-line models. CKS1B expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, CKS1B is differentially expressed in 17, with the highest sampling consensus in BLCA. Additionally, CKS1B protein abundance shows 24,859 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight ACC, BLCA, and LUAD as cancer lineages where CKS1B 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 CKS1B — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CKS1B survival associations across molecular data types. CKS1B RNA expression shows survival associations in the most cancer types (28), followed by mutation status (3) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CKS1B RNA expression–survival associations across cancer types. High CKS1B expression shows unfavorable associations in ACC, KIRP, UVM, LUAD, LIHC and BRCA. The ACC 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 ACC as the clearest survival context for CKS1B RNA expression.
This table summarizes CKS1B tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 17, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CKS1B. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CKS1B shows higher tumor expression in BLCA, HNSC, KIRC, LUAD, COAD and STAD. The BLCA box plot shows higher CKS1B RNA expression in tumor versus normal tissue (log2 FC = +2.295, t-test p < 0.001).
This table shows molecular features associated with CKS1B in patient tissues and cancer cell lines. In patient samples, CKS1B shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, CKS1B RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and SOFT_TISSUE.
