Q-omics provides the consensus-scored DMD profile across patient tissues and cancer cell-line models. DMD 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, DMD is differentially expressed in 15, with the highest sampling consensus in LUAD. Additionally, DMD protein abundance shows 28,630 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRP, and LUAD as cancer lineages where DMD 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 DMD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DMD survival associations across molecular data types. DMD RNA expression shows survival associations in the most cancer types (27), followed by mutation status (14) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible DMD RNA expression–survival associations across cancer types. High DMD expression shows unfavorable associations in KIRP and LGG, but favorable associations in KIRC, UCS, LUAD and BRCA. 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 DMD RNA expression.
This table summarizes DMD tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 7. The strongest signals are observed in LUAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for DMD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DMD shows lower tumor expression in LUAD, COAD, BLCA, LUSC, BRCA and UCEC. The LUAD box plot shows higher DMD RNA expression in normal versus tumor tissue (log2 FC = −1.505, t-test p < 0.001).
This table shows molecular features associated with DMD in patient tissues and cancer cell lines. In patient samples, DMD shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, DMD 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 BONE and LARGE_INTESTINE.
