Q-omics provides the consensus-scored DCD profile across patient tissues and cancer cell-line models. DCD expression is associated with patient survival in 16 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, DCD is differentially expressed in 5, with the highest sampling consensus in KIRC. Additionally, DCD protein abundance shows 7,045 significant protein co-abundance associations, with the highest sampling consensus in UCEC. Together, these results highlight KIRC, and UCEC as cancer lineages where DCD 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 DCD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DCD survival associations across molecular data types. DCD RNA expression shows survival associations in the most cancer types (16), followed by mutation status (4) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible DCD RNA expression–survival associations across cancer types. High DCD expression shows unfavorable associations in KIRC, THCA, UVM, DLBC and UCEC, but favorable associations in SCLC. The KIRC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for DCD RNA expression.
This table summarizes DCD tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 5, while mass-spec protein shows differences in 2. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for DCD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DCD shows lower tumor expression in KIRC, KICH, THCA, BRCA and KIRP. The KIRC box plot shows higher DCD RNA expression in normal versus tumor tissue (log2 FC = −0.172, t-test p < 0.001).
This table shows molecular features associated with DCD in patient tissues and cancer cell lines. In patient samples, DCD shows the broadest associations at the RNA and protein expression levels, with UCEC recurring as the lineage with the largest associated feature set. In cancer cell lines, DCD 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 BLOOD_Lymphoma and LARGE_INTESTINE.
