Q-omics provides the consensus-scored MREG profile across patient tissues and cancer cell-line models. MREG expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, MREG is differentially expressed in 12, with the highest sampling consensus in THCA. Additionally, MREG RNA expression shows 18,814 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRP, THCA, and UVM as cancer lineages where MREG 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 MREG — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MREG survival associations across molecular data types. MREG RNA expression shows survival associations in the most cancer types (26), followed by mutation status (5) 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 MREG RNA expression–survival associations across cancer types. High MREG expression shows unfavorable associations in KIRP, ACC and LGG, but favorable associations in OV, KIRC and MESO. 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 MREG RNA expression.
This table summarizes MREG 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 2. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for MREG. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MREG shows higher tumor expression in THCA, LIHC, BLCA, READ, COAD and UCEC. The THCA box plot shows higher MREG RNA expression in tumor versus normal tissue (log2 FC = +0.874, t-test p < 0.001).
This table shows molecular features associated with MREG in patient tissues and cancer cell lines. In patient samples, MREG shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, MREG 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 LARGE_INTESTINE and BONE.
