Q-omics provides the consensus-scored MTDH profile across patient tissues and cancer cell-line models. MTDH expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, MTDH is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, MTDH protein abundance shows 20,845 significant protein co-abundance associations, with the highest sampling consensus in BRCA. Together, these results highlight UVM, HNSC, and BRCA as cancer lineages where MTDH 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 MTDH — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MTDH survival associations across molecular data types. MTDH RNA expression shows survival associations in the most cancer types (25), followed by mutation status (5) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MTDH RNA expression–survival associations across cancer types. High MTDH expression shows unfavorable associations in UVM, CESC, HNSC, KIRP, LUAD and BRCA. The UVM 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 UVM as the clearest survival context for MTDH RNA expression.
This table summarizes MTDH 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 6. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for MTDH. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MTDH shows higher tumor expression in HNSC, KIRC, STAD, COAD, LIHC and KIRP. The HNSC box plot shows higher MTDH RNA expression in tumor versus normal tissue (log2 FC = +1.030, t-test p < 0.001).
This table shows molecular features associated with MTDH in patient tissues and cancer cell lines. In patient samples, MTDH shows the broadest associations at the RNA and protein expression levels, with BRCA recurring as the lineage with the largest associated feature set. In cancer cell lines, MTDH RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUSC, while CRISPR and shRNA rows add functional-dependency signals in KIDNEY and BLOOD_Lymphoma.
