Q-omics provides the consensus-scored CLNK profile across patient tissues and cancer cell-line models. CLNK expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, CLNK is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, CLNK RNA expression shows 15,381 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight SKCM, KIRC, and UVM as cancer lineages where CLNK 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 CLNK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CLNK survival associations across molecular data types. CLNK RNA expression shows survival associations in the most cancer types (25), followed by mutation status (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CLNK RNA expression–survival associations across cancer types. High CLNK expression shows unfavorable associations in UVM, but favorable associations in SKCM, HNSC, BRCA, SCLC and BLCA. The SKCM 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 SKCM as the clearest survival context for CLNK RNA expression.
This table summarizes CLNK tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, 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 CLNK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CLNK shows lower tumor expression in KIRC and KIRP and higher tumor expression in KICH, LUAD, STAD and BRCA. The KIRC box plot shows higher CLNK RNA expression in normal versus tumor tissue (log2 FC = −2.090, t-test p < 0.001).
This table shows molecular features associated with CLNK in patient tissues and cancer cell lines. In patient samples, CLNK 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, CLNK 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 SOFT_TISSUE and LARGE_INTESTINE.
