Q-omics provides the consensus-scored MT1M profile across patient tissues and cancer cell-line models. MT1M expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, MT1M is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, MT1M RNA expression shows 12,721 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight MESO, KIRC, and LSCC as cancer lineages where MT1M 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 MT1M — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MT1M survival associations across molecular data types. MT1M RNA expression shows survival associations in the most cancer types (22), followed by mutation status (9) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MT1M RNA expression–survival associations across cancer types. High MT1M expression shows unfavorable associations in LGG, UCS and THCA, but favorable associations in MESO, LUSC and PRAD. The MESO Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .001). Together, the overview and detailed table identify MESO as the clearest survival context for MT1M RNA expression.
This table summarizes MT1M 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 3. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for MT1M. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MT1M shows lower tumor expression in KIRC, COAD, KICH, KIRP, THCA and BLCA. The KIRC box plot shows higher MT1M RNA expression in normal versus tumor tissue (log2 FC = −3.066, t-test p < 0.001).
This table shows molecular features associated with MT1M in patient tissues and cancer cell lines. In patient samples, MT1M 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, MT1M RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD.
