Q-omics provides the consensus-scored MSRA profile across patient tissues and cancer cell-line models. MSRA expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, MSRA is differentially expressed in 17, with the highest sampling consensus in KIRP. Additionally, MSRA protein abundance shows 21,995 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, KIRP, and LSCC as cancer lineages where MSRA 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 MSRA — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MSRA survival associations across molecular data types. MSRA RNA expression shows survival associations in the most cancer types (27), followed by mutation status (2) 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 MSRA RNA expression–survival associations across cancer types. High MSRA expression shows unfavorable associations in KICH, but favorable associations in KIRC, ACC, THCA, COAD and UVM. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for MSRA RNA expression.
This table summarizes MSRA tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 17, while mass-spec protein shows differences in 6. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for MSRA. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MSRA shows lower tumor expression in KIRP, HNSC, COAD, BLCA, KICH and LUSC. The KIRP box plot shows higher MSRA RNA expression in normal versus tumor tissue (log2 FC = −1.885, t-test p < 0.001).
This table shows molecular features associated with MSRA in patient tissues and cancer cell lines. In patient samples, MSRA shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, MSRA RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in BREAST and CNS.
