Q-omics provides the consensus-scored RRAD profile across patient tissues and cancer cell-line models. RRAD expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, RRAD is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, RRAD protein abundance shows 21,004 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight MESO, KIRC, and LUAD as cancer lineages where RRAD 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 RRAD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes RRAD survival associations across molecular data types. RRAD RNA expression shows survival associations in the most cancer types (20), followed by mutation status (3) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible RRAD RNA expression–survival associations across cancer types. High RRAD expression shows unfavorable associations in MESO, LUSC and UVM, but favorable associations in CESC, ACC and SKCM. 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 RRAD RNA expression.
This table summarizes RRAD 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 5. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for RRAD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. RRAD shows lower tumor expression in BLCA, LUSC, LUAD, KICH and UCEC and higher tumor expression in KIRC. The KIRC box plot shows higher RRAD RNA expression in tumor versus normal tissue (log2 FC = +1.639, t-test p < 0.001).
This table shows molecular features associated with RRAD in patient tissues and cancer cell lines. In patient samples, RRAD 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, RRAD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BONE.
