Q-omics provides the consensus-scored CCL5 profile across patient tissues and cancer cell-line models. CCL5 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, CCL5 is differentially expressed in 9, with the highest sampling consensus in HNSC. Additionally, CCL5 RNA expression shows 19,431 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight SKCM, HNSC, and LSCC as cancer lineages where CCL5 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 CCL5 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CCL5 survival associations across molecular data types. CCL5 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (2) and 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 CCL5 RNA expression–survival associations across cancer types. High CCL5 expression shows unfavorable associations in UVM and KIRP, but favorable associations in SKCM, CESC, UCEC 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 CCL5 RNA expression.
This table summarizes CCL5 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 5. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CCL5. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CCL5 shows lower tumor expression in COAD, LUSC and LUAD and higher tumor expression in HNSC, KIRC and KIRP. The HNSC box plot shows higher CCL5 RNA expression in tumor versus normal tissue (log2 FC = +1.574, t-test p < 0.001).
This table shows molecular features associated with CCL5 in patient tissues and cancer cell lines. In patient samples, CCL5 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, CCL5 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and BLOOD_Leukemia.
