Q-omics provides the consensus-scored HADHA profile across patient tissues and cancer cell-line models. HADHA expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, HADHA is differentially expressed in 11, with the highest sampling consensus in COAD. Additionally, HADHA protein abundance shows 22,612 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight KIRC, COAD, and HNSC as cancer lineages where HADHA 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 HADHA — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HADHA survival associations across molecular data types. HADHA RNA expression shows survival associations in the most cancer types (20), followed by mutation status (5) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible HADHA RNA expression–survival associations across cancer types. High HADHA expression shows unfavorable associations in ACC, BLCA, CESC and LIHC, but favorable associations in KIRC and LGG. 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 HADHA RNA expression.
This table summarizes HADHA tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 6. The strongest signals are observed in COAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for HADHA. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HADHA shows lower tumor expression in COAD, THCA, READ, BRCA and KICH and higher tumor expression in LIHC. The COAD box plot shows higher HADHA RNA expression in normal versus tumor tissue (log2 FC = −0.836, t-test p < 0.001).
This table shows molecular features associated with HADHA in patient tissues and cancer cell lines. In patient samples, HADHA shows the broadest associations at the RNA and protein expression levels, with HNSC recurring as the lineage with the largest associated feature set. In cancer cell lines, HADHA RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and BLOOD_Leukemia.
