Q-omics provides the consensus-scored CCNK profile across patient tissues and cancer cell-line models. CCNK expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CCNK is differentially expressed in 11, with the highest sampling consensus in HNSC. Additionally, CCNK protein abundance shows 35,903 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, HNSC, and LSCC as cancer lineages where CCNK 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 CCNK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CCNK survival associations across molecular data types. CCNK RNA expression shows survival associations in the most cancer types (25), followed by mutation status (1) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CCNK RNA expression–survival associations across cancer types. High CCNK expression shows unfavorable associations in MESO, PAAD, CESC and ACC, but favorable associations in KIRC and SCLC. The KIRC 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 KIRC as the clearest survival context for CCNK RNA expression.
This table summarizes CCNK tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 10. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CCNK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CCNK shows lower tumor expression in THCA and higher tumor expression in HNSC, BLCA, STAD, LUSC and KIRP. The HNSC box plot shows higher CCNK RNA expression in tumor versus normal tissue (log2 FC = +0.744, t-test p < 0.001).
This table shows molecular features associated with CCNK in patient tissues and cancer cell lines. In patient samples, CCNK 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, CCNK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BLOOD_Leukemia.
