Q-omics provides the consensus-scored DHDH profile across patient tissues and cancer cell-line models. DHDH expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, DHDH is differentially expressed in 14, with the highest sampling consensus in THCA. Additionally, DHDH protein abundance shows 18,256 significant protein co-abundance associations, with the highest sampling consensus in CCRCC. Together, these results highlight KIRC, THCA, and CCRCC as cancer lineages where DHDH 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 DHDH — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DHDH survival associations across molecular data types. DHDH RNA expression shows survival associations in the most cancer types (21), followed by mutation status (4) 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 DHDH RNA expression–survival associations across cancer types. High DHDH expression shows unfavorable associations in ACC, UVM, LIHC and THYM, but favorable associations in KIRC and KIRP. 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 DHDH RNA expression.
This table summarizes DHDH 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 5. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for DHDH. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DHDH shows lower tumor expression in KICH and higher tumor expression in THCA, HNSC, BLCA, COAD and LIHC. The THCA box plot shows higher DHDH RNA expression in tumor versus normal tissue (log2 FC = +2.607, t-test p < 0.001).
This table shows molecular features associated with DHDH in patient tissues and cancer cell lines. In patient samples, DHDH shows the broadest associations at the RNA and protein expression levels, with CCRCC recurring as the lineage with the largest associated feature set. In cancer cell lines, DHDH RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BLOOD_Leukemia.
