Q-omics provides the consensus-scored H6PD profile across patient tissues and cancer cell-line models. H6PD expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, H6PD is differentially expressed in 9, with the highest sampling consensus in KIRC. Additionally, H6PD protein abundance shows 31,855 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight MESO, KIRC, and GBM as cancer lineages where H6PD 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 H6PD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes H6PD survival associations across molecular data types. H6PD RNA expression shows survival associations in the most cancer types (22), followed by mutation status (6) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible H6PD RNA expression–survival associations across cancer types. High H6PD expression shows unfavorable associations in LGG, but favorable associations in MESO, HNSC, KIRC, BRCA and CHOL. The MESO 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 MESO as the clearest survival context for H6PD RNA expression.
This table summarizes H6PD tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 10. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for H6PD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. H6PD shows lower tumor expression in UCEC, BRCA and KICH and higher tumor expression in KIRC, KIRP and STAD. The KIRC box plot shows higher H6PD RNA expression in tumor versus normal tissue (log2 FC = +1.096, t-test p < 0.001).
This table shows molecular features associated with H6PD in patient tissues and cancer cell lines. In patient samples, H6PD shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, H6PD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and CNS.
