Q-omics provides the consensus-scored HADH profile across patient tissues and cancer cell-line models. HADH expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, HADH is differentially expressed in 15, with the highest sampling consensus in KIRP. Additionally, HADH protein abundance shows 23,770 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRC, KIRP, and PDAC as cancer lineages where HADH 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 HADH — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HADH survival associations across molecular data types. HADH RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) 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 HADH RNA expression–survival associations across cancer types. High HADH expression shows unfavorable associations in KICH, but favorable associations in KIRC, KIRP, UCEC, READ and BRCA. 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 HADH RNA expression.
This table summarizes HADH tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for HADH. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HADH shows lower tumor expression in KIRP, KIRC, COAD, HNSC, THCA and KICH. The KIRP box plot shows higher HADH RNA expression in normal versus tumor tissue (log2 FC = −1.915, t-test p < 0.001).
This table shows molecular features associated with HADH in patient tissues and cancer cell lines. In patient samples, HADH shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, HADH 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 SKIN and BLOOD_Leukemia.
