Q-omics provides the consensus-scored WNK3 profile across patient tissues and cancer cell-line models. WNK3 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, WNK3 is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, WNK3 RNA expression shows 19,399 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight HNSC, KIRC, and UVM as cancer lineages where WNK3 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 WNK3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes WNK3 survival associations across molecular data types. WNK3 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (9) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible WNK3 RNA expression–survival associations across cancer types. High WNK3 expression shows unfavorable associations in UCEC and KIRP, but favorable associations in HNSC, ACC, PAAD and UCS. The HNSC 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 HNSC as the clearest survival context for WNK3 RNA expression.
This table summarizes WNK3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 3. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for WNK3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. WNK3 shows lower tumor expression in KIRC, KIRP and THCA and higher tumor expression in KICH, LUSC and LUAD. The KIRC box plot shows higher WNK3 RNA expression in normal versus tumor tissue (log2 FC = −1.188, t-test p < 0.001).
This table shows molecular features associated with WNK3 in patient tissues and cancer cell lines. In patient samples, WNK3 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, WNK3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and BONE.
