Q-omics provides the consensus-scored TMC4 profile across patient tissues and cancer cell-line models. TMC4 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, TMC4 is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, TMC4 RNA expression shows 16,054 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KIRP, KIRC, and TGCT as cancer lineages where TMC4 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 TMC4 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TMC4 survival associations across molecular data types. TMC4 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (6) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TMC4 RNA expression–survival associations across cancer types. High TMC4 expression shows unfavorable associations in LUSC and OV, but favorable associations in KIRP, MESO, UCS and STAD. The KIRP Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .002). Together, the overview and detailed table identify KIRP as the clearest survival context for TMC4 RNA expression.
This table summarizes TMC4 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, 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 TMC4. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TMC4 shows lower tumor expression in KIRC, KIRP, COAD and LUSC and higher tumor expression in BRCA and STAD. The KIRC box plot shows higher TMC4 RNA expression in normal versus tumor tissue (log2 FC = −3.644, t-test p < 0.001).
This table shows molecular features associated with TMC4 in patient tissues and cancer cell lines. In patient samples, TMC4 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, TMC4 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 BREAST and LUNG_NSCLC_LUAD.
