Q-omics provides the consensus-scored CCL25 profile across patient tissues and cancer cell-line models. CCL25 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, CCL25 is differentially expressed in 9, with the highest sampling consensus in LUAD. Additionally, CCL25 RNA expression shows 11,941 significant gene co-expression associations, with the highest sampling consensus in ESCA. Together, these results highlight HNSC, LUAD, and ESCA as cancer lineages where CCL25 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 CCL25 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CCL25 survival associations across molecular data types. CCL25 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (1) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CCL25 RNA expression–survival associations across cancer types. High CCL25 expression shows unfavorable associations in KIRP, KIRC and LGG, but favorable associations in HNSC, SKCM and CESC. 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 CCL25 RNA expression.
This table summarizes CCL25 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 2. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CCL25. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CCL25 shows higher tumor expression in LUAD, KIRC, KICH, HNSC, LIHC and LUSC. The LUAD box plot shows higher CCL25 RNA expression in tumor versus normal tissue (log2 FC = +0.507, t-test p < 0.001).
This table shows molecular features associated with CCL25 in patient tissues and cancer cell lines. In patient samples, CCL25 shows the broadest associations at the RNA and protein expression levels, with ESCA recurring as the lineage with the largest associated feature set. In cancer cell lines, CCL25 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BLOOD_Leukemia.
