Q-omics provides the consensus-scored TNFRSF4 profile across patient tissues and cancer cell-line models. TNFRSF4 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, TNFRSF4 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, TNFRSF4 RNA expression shows 14,917 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight HNSC, KIRC, and LSCC as cancer lineages where TNFRSF4 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 TNFRSF4 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TNFRSF4 survival associations across molecular data types. TNFRSF4 RNA expression shows survival associations in the most cancer types (24), 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 TNFRSF4 RNA expression–survival associations across cancer types. High TNFRSF4 expression shows unfavorable associations in UVM, KIRP and UCS, but favorable associations in HNSC, SKCM and LUAD. The HNSC 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 HNSC as the clearest survival context for TNFRSF4 RNA expression.
This table summarizes TNFRSF4 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for TNFRSF4. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TNFRSF4 shows higher tumor expression in KIRC, HNSC, COAD, THCA, STAD and LIHC. The KIRC box plot shows higher TNFRSF4 RNA expression in tumor versus normal tissue (log2 FC = +2.704, t-test p < 0.001).
This table shows molecular features associated with TNFRSF4 in patient tissues and cancer cell lines. In patient samples, TNFRSF4 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, TNFRSF4 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 LARGE_INTESTINE and BLOOD_Lymphoma.
