Q-omics provides the consensus-scored TNMD profile across patient tissues and cancer cell-line models. TNMD expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, TNMD is differentially expressed in 10, with the highest sampling consensus in HNSC. Additionally, TNMD RNA expression shows 10,688 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KIRC, HNSC, and TGCT as cancer lineages where TNMD 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 TNMD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TNMD survival associations across molecular data types. TNMD RNA expression shows survival associations in the most cancer types (19), followed by mutation status (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TNMD RNA expression–survival associations across cancer types. High TNMD expression shows unfavorable associations in SCLC, ACC, STAD and UVM, but favorable associations in KIRC and READ. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .004). Together, the overview and detailed table identify KIRC as the clearest survival context for TNMD RNA expression.
This table summarizes TNMD tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 1. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for TNMD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TNMD shows lower tumor expression in HNSC, KICH, KIRP, BRCA, UCEC and STAD. The HNSC box plot shows higher TNMD RNA expression in normal versus tumor tissue (log2 FC = −0.635, t-test p < 0.001).
This table shows molecular features associated with TNMD in patient tissues and cancer cell lines. In patient samples, TNMD 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, TNMD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Myeloma and BLOOD_Leukemia.
