Q-omics provides the consensus-scored TNFRSF25 profile across patient tissues and cancer cell-line models. TNFRSF25 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, TNFRSF25 is differentially expressed in 17, with the highest sampling consensus in KIRC. Additionally, TNFRSF25 RNA expression shows 17,422 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight SKCM, KIRC, and UVM as cancer lineages where TNFRSF25 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 TNFRSF25 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TNFRSF25 survival associations across molecular data types. TNFRSF25 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TNFRSF25 RNA expression–survival associations across cancer types. High TNFRSF25 expression shows unfavorable associations in KIRC, ACC, PRAD and LGG, but favorable associations in SKCM and HNSC. The SKCM 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 SKCM as the clearest survival context for TNFRSF25 RNA expression.
This table summarizes TNFRSF25 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 17. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for TNFRSF25. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TNFRSF25 shows lower tumor expression in KICH and higher tumor expression in KIRC, THCA, LIHC, BLCA and HNSC. The KIRC box plot shows higher TNFRSF25 RNA expression in tumor versus normal tissue (log2 FC = +0.816, t-test p < 0.001).
This table shows molecular features associated with TNFRSF25 in patient tissues and cancer cell lines. In patient samples, TNFRSF25 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, TNFRSF25 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 BLOOD_Myeloma and BLOOD_Leukemia.
