Q-omics provides the consensus-scored MT1F profile across patient tissues and cancer cell-line models. MT1F expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, MT1F is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, MT1F RNA expression shows 13,842 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight HNSC, KIRC, and TGCT as cancer lineages where MT1F 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 MT1F — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MT1F survival associations across molecular data types. MT1F RNA expression shows survival associations in the most cancer types (22), followed by mutation status (1) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MT1F RNA expression–survival associations across cancer types. High MT1F expression shows unfavorable associations in HNSC, UCS, KIRC and LGG, but favorable associations in READ and MESO. The HNSC 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 HNSC as the clearest survival context for MT1F RNA expression.
This table summarizes MT1F 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 5. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for MT1F. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MT1F shows lower tumor expression in KIRC, KICH, THCA, KIRP and COAD and higher tumor expression in HNSC. The KIRC box plot shows higher MT1F RNA expression in normal versus tumor tissue (log2 FC = −2.781, t-test p < 0.001).
This table shows molecular features associated with MT1F in patient tissues and cancer cell lines. In patient samples, MT1F shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, MT1F RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and OVARY.
