Q-omics provides the consensus-scored MTRR profile across patient tissues and cancer cell-line models. MTRR expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, MTRR is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, MTRR RNA expression shows 19,643 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, HNSC, and UVM as cancer lineages where MTRR 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 MTRR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MTRR survival associations across molecular data types. MTRR RNA expression shows survival associations in the most cancer types (26), followed by mutation status (9) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MTRR RNA expression–survival associations across cancer types. High MTRR expression shows unfavorable associations in CESC, LGG, LIHC and KICH, but favorable associations in KIRC and LUAD. 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 MTRR RNA expression.
This table summarizes MTRR 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 KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for MTRR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MTRR shows lower tumor expression in THCA, LUSC, LUAD and KICH and higher tumor expression in HNSC and KIRC. The HNSC box plot shows higher MTRR RNA expression in tumor versus normal tissue (log2 FC = +0.815, t-test p < 0.001).
This table shows molecular features associated with MTRR in patient tissues and cancer cell lines. In patient samples, MTRR 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, MTRR 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 LUNG_NSCLC_LUAD and UPPER_AERODIGESTIVE_TRACT.
