Q-omics provides the consensus-scored DSC3 profile across patient tissues and cancer cell-line models. DSC3 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, DSC3 is differentially expressed in 10, with the highest sampling consensus in HNSC. Additionally, DSC3 protein abundance shows 22,767 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight MESO, and HNSC as cancer lineages where DSC3 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 DSC3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DSC3 survival associations across molecular data types. DSC3 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (11) 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 DSC3 RNA expression–survival associations across cancer types. High DSC3 expression shows unfavorable associations in MESO, BLCA, STAD and SKCM, but favorable associations in LUSC and CESC. The MESO 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 MESO as the clearest survival context for DSC3 RNA expression.
This table summarizes DSC3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 10. The strongest signals are observed in HNSC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for DSC3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DSC3 shows lower tumor expression in KICH and BRCA and higher tumor expression in HNSC, LUSC, COAD and THCA. The HNSC box plot shows higher DSC3 RNA expression in tumor versus normal tissue (log2 FC = +1.184, t-test p < 0.001).
This table shows molecular features associated with DSC3 in patient tissues and cancer cell lines. In patient samples, DSC3 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, DSC3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in BREAST and LARGE_INTESTINE.