Q-omics provides the consensus-scored CDK16 profile across patient tissues and cancer cell-line models. CDK16 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in LIHC. Among the 18 cancer types available for tumor–normal comparison, CDK16 is differentially expressed in 18, with the highest sampling consensus in COAD. Additionally, CDK16 protein abundance shows 22,913 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight LIHC, COAD, and GBM as cancer lineages where CDK16 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 CDK16 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CDK16 survival associations across molecular data types. CDK16 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (2) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CDK16 RNA expression–survival associations across cancer types. High CDK16 expression shows unfavorable associations in LIHC, ACC, KICH, KIRC, ESCA and MESO. The LIHC 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 LIHC as the clearest survival context for CDK16 RNA expression.
This table summarizes CDK16 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 18, while mass-spec protein shows differences in 9. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CDK16. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CDK16 shows higher tumor expression in COAD, HNSC, LIHC, BLCA, LUAD and LUSC. The COAD box plot shows higher CDK16 RNA expression in tumor versus normal tissue (log2 FC = +0.868, t-test p < 0.001).
This table shows molecular features associated with CDK16 in patient tissues and cancer cell lines. In patient samples, CDK16 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, CDK16 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 LUNG_SCLC.
