Q-omics provides the consensus-scored NLK profile across patient tissues and cancer cell-line models. NLK expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, NLK is differentially expressed in 14, with the highest sampling consensus in BLCA. Additionally, NLK RNA expression shows 20,711 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight ACC, BLCA, and UVM as cancer lineages where NLK 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 NLK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NLK survival associations across molecular data types. NLK RNA expression shows survival associations in the most cancer types (28), followed by mutation status (7) 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 NLK RNA expression–survival associations across cancer types. High NLK expression shows unfavorable associations in ACC, MESO, UVM and KIRP, but favorable associations in READ and KIRC. The ACC 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 ACC as the clearest survival context for NLK RNA expression.
This table summarizes NLK 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 2. The strongest signals are observed in HNSC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for NLK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NLK shows lower tumor expression in KICH and THCA and higher tumor expression in BLCA, HNSC, LIHC and STAD. The BLCA box plot shows higher NLK RNA expression in tumor versus normal tissue (log2 FC = +1.118, t-test p < 0.001).
This table shows molecular features associated with NLK in patient tissues and cancer cell lines. In patient samples, NLK 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, NLK 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 BLOOD_Leukemia and LARGE_INTESTINE.
