Q-omics provides the consensus-scored CCL17 profile across patient tissues and cancer cell-line models. CCL17 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in CESC. Among the 18 cancer types available for tumor–normal comparison, CCL17 is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, CCL17 protein abundance shows 25,003 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight CESC, KIRC, and PDAC as cancer lineages where CCL17 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 CCL17 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CCL17 survival associations across molecular data types. CCL17 RNA expression shows survival associations in the most cancer types (22), followed by mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CCL17 RNA expression–survival associations across cancer types. High CCL17 expression shows favorable associations in CESC, BLCA, HNSC, UCEC, CHOL and SARC. The CESC 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 CESC as the clearest survival context for CCL17 RNA expression.
This table summarizes CCL17 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for CCL17. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CCL17 shows lower tumor expression in LUSC and KICH and higher tumor expression in KIRC, THCA, BLCA and BRCA. The KIRC box plot shows higher CCL17 RNA expression in tumor versus normal tissue (log2 FC = +1.295, t-test p < 0.001).
This table shows molecular features associated with CCL17 in patient tissues and cancer cell lines. In patient samples, CCL17 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, CCL17 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and UPPER_AERODIGESTIVE_TRACT.
