Q-omics provides the consensus-scored CKS2 profile across patient tissues and cancer cell-line models. CKS2 expression is associated with patient survival in 32 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, CKS2 is differentially expressed in 16, with the highest sampling consensus in HNSC. Additionally, CKS2 RNA expression shows 23,192 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight MESO, HNSC, and LSCC as cancer lineages where CKS2 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 CKS2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CKS2 survival associations across molecular data types. CKS2 RNA expression shows survival associations in the most cancer types (32), followed by mutation status (2) 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 CKS2 RNA expression–survival associations across cancer types. High CKS2 expression shows unfavorable associations in MESO, ACC, KIRP, UVM, LIHC and LUAD. The MESO 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 MESO as the clearest survival context for CKS2 RNA expression.
This table summarizes CKS2 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 1. The strongest signals are observed in HNSC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for CKS2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CKS2 shows higher tumor expression in HNSC, BLCA, COAD, KIRP, KIRC and LIHC. The HNSC box plot shows higher CKS2 RNA expression in tumor versus normal tissue (log2 FC = +2.119, t-test p < 0.001).
This table shows molecular features associated with CKS2 in patient tissues and cancer cell lines. In patient samples, CKS2 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, CKS2 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 LUNG_SCLC and BLOOD_Leukemia.
