Q-omics provides the consensus-scored OMD profile across patient tissues and cancer cell-line models. OMD expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, OMD is differentially expressed in 12, with the highest sampling consensus in COAD. Additionally, OMD protein abundance shows 23,938 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRP, COAD, and PDAC as cancer lineages where OMD 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 OMD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes OMD survival associations across molecular data types. OMD RNA expression shows survival associations in the most cancer types (19), followed by mutation status (4) 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 OMD RNA expression–survival associations across cancer types. High OMD expression shows unfavorable associations in KIRP, BLCA, ACC and STAD, but favorable associations in LIHC and CHOL. 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 OMD RNA expression.
This table summarizes OMD 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 8. The strongest signals are observed in COAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for OMD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. OMD shows lower tumor expression in COAD, KICH, THCA, BLCA, KIRC and KIRP. The COAD box plot shows higher OMD RNA expression in normal versus tumor tissue (log2 FC = −1.767, t-test p < 0.001).
This table shows molecular features associated with OMD in patient tissues and cancer cell lines. In patient samples, OMD 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, OMD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Myeloma and LUNG_SCLC.
