Q-omics provides the consensus-scored CLK3 profile across patient tissues and cancer cell-line models. CLK3 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in COAD. Among the 18 cancer types available for tumor–normal comparison, CLK3 is differentially expressed in 11, with the highest sampling consensus in HNSC. Additionally, CLK3 RNA expression shows 19,627 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight COAD, HNSC, and ACC as cancer lineages where CLK3 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 CLK3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CLK3 survival associations across molecular data types. CLK3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (5) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CLK3 RNA expression–survival associations across cancer types. High CLK3 expression shows unfavorable associations in COAD, ACC, KIRP, CESC and MESO, but favorable associations in UCEC. The COAD 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 COAD as the clearest survival context for CLK3 RNA expression.
This table summarizes CLK3 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 2. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CLK3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CLK3 shows lower tumor expression in THCA and higher tumor expression in HNSC, KIRC, LIHC, STAD and CHOL. The HNSC box plot shows higher CLK3 RNA expression in tumor versus normal tissue (log2 FC = +0.456, t-test p < 0.001).
This table shows molecular features associated with CLK3 in patient tissues and cancer cell lines. In patient samples, CLK3 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, CLK3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Myeloma, while CRISPR and shRNA rows add functional-dependency signals in LIVER and BLOOD_Leukemia.
