Q-omics provides the consensus-scored CLCNKA profile across patient tissues and cancer cell-line models. CLCNKA expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, CLCNKA is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, CLCNKA RNA expression shows 15,049 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight UVM, and KIRC as cancer lineages where CLCNKA 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 CLCNKA — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CLCNKA survival associations across molecular data types. CLCNKA RNA expression shows survival associations in the most cancer types (19), followed by mutation status (8) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CLCNKA RNA expression–survival associations across cancer types. High CLCNKA expression shows unfavorable associations in UVM, KIRC, LGG, LAML and LIHC, but favorable associations in KIRP. The UVM 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 UVM as the clearest survival context for CLCNKA RNA expression.
This table summarizes CLCNKA tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 2. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CLCNKA. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CLCNKA shows lower tumor expression in KIRC, KIRP, THCA, STAD and COAD and higher tumor expression in LIHC. The KIRC box plot shows higher CLCNKA RNA expression in normal versus tumor tissue (log2 FC = −6.268, t-test p < 0.001).
This table shows molecular features associated with CLCNKA in patient tissues and cancer cell lines. In patient samples, CLCNKA shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, CLCNKA RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in KIDNEY and LARGE_INTESTINE.
