Q-omics provides the consensus-scored CHDH profile across patient tissues and cancer cell-line models. CHDH expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, CHDH is differentially expressed in 12, with the highest sampling consensus in KICH. Additionally, CHDH protein abundance shows 20,034 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRP, KICH, and LSCC as cancer lineages where CHDH 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 CHDH — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CHDH survival associations across molecular data types. CHDH RNA expression shows survival associations in the most cancer types (27), followed by mutation status (6) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CHDH RNA expression–survival associations across cancer types. High CHDH expression shows favorable associations in KIRP, KIRC, HNSC, COAD, SKCM and BRCA. The KIRP 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 KIRP as the clearest survival context for CHDH RNA expression.
This table summarizes CHDH tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 5. The strongest signals are observed in KICH for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CHDH. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CHDH shows lower tumor expression in KICH, HNSC and KIRC and higher tumor expression in STAD, BLCA and COAD. The KICH box plot shows higher CHDH RNA expression in normal versus tumor tissue (log2 FC = −3.531, t-test p < 0.001).
This table shows molecular features associated with CHDH in patient tissues and cancer cell lines. In patient samples, CHDH 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, CHDH RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in CNS and BREAST.
