Q-omics provides the consensus-scored DCN profile across patient tissues and cancer cell-line models. DCN expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, DCN is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, DCN protein abundance shows 31,949 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRP, KIRC, and PDAC as cancer lineages where DCN 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 DCN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DCN survival associations across molecular data types. DCN RNA expression shows survival associations in the most cancer types (23), followed by mutation status (7) 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 DCN RNA expression–survival associations across cancer types. High DCN expression shows unfavorable associations in KIRP, KIRC and ACC, but favorable associations in LUAD, DLBC and UCEC. The KIRP 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 KIRP as the clearest survival context for DCN RNA expression.
This table summarizes DCN 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 7. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for DCN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DCN shows lower tumor expression in KIRC, BLCA, COAD, KICH, THCA and KIRP. The KIRC box plot shows higher DCN RNA expression in normal versus tumor tissue (log2 FC = −3.838, t-test p < 0.001).
This table shows molecular features associated with DCN in patient tissues and cancer cell lines. In patient samples, DCN 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, DCN 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 BLOOD_Leukemia and BONE.
