Q-omics provides the consensus-scored KHK profile across patient tissues and cancer cell-line models. KHK expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, KHK is differentially expressed in 14, with the highest sampling consensus in KIRP. Additionally, KHK RNA expression shows 17,364 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, KIRP, and LSCC as cancer lineages where KHK 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 KHK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes KHK survival associations across molecular data types. KHK RNA expression shows survival associations in the most cancer types (27), followed by mutation status (2) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible KHK RNA expression–survival associations across cancer types. High KHK expression shows unfavorable associations in UCEC, MESO and CHOL, but favorable associations in KIRC, STAD and UVM. The KIRC 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 KIRC as the clearest survival context for KHK RNA expression.
This table summarizes KHK 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 4. The strongest signals are observed in KIRP for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for KHK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. KHK shows lower tumor expression in KIRP, KICH, UCEC and CHOL and higher tumor expression in COAD and KIRC. The KIRP box plot shows higher KHK RNA expression in normal versus tumor tissue (log2 FC = −3.002, t-test p < 0.001).
This table shows molecular features associated with KHK in patient tissues and cancer cell lines. In patient samples, KHK shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, KHK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in CNS and BONE.
