Q-omics provides the consensus-scored TMED4 profile across patient tissues and cancer cell-line models. TMED4 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, TMED4 is differentially expressed in 14, with the highest sampling consensus in COAD. Additionally, TMED4 protein abundance shows 20,265 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRC, COAD, and PDAC as cancer lineages where TMED4 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 TMED4 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TMED4 survival associations across molecular data types. TMED4 RNA expression shows survival associations in the most cancer types (25), followed by 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 TMED4 RNA expression–survival associations across cancer types. High TMED4 expression shows unfavorable associations in CESC, UVM, HNSC, LGG and COAD, but favorable associations in KIRC. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for TMED4 RNA expression.
This table summarizes TMED4 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 6. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for TMED4. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TMED4 shows higher tumor expression in COAD, HNSC, BLCA, LIHC, LUAD and BRCA. The COAD box plot shows higher TMED4 RNA expression in tumor versus normal tissue (log2 FC = +0.793, t-test p < 0.001).
This table shows molecular features associated with TMED4 in patient tissues and cancer cell lines. In patient samples, TMED4 shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, TMED4 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in STOMACH and UPPER_AERODIGESTIVE_TRACT.
