Q-omics provides the consensus-scored CCL22 profile across patient tissues and cancer cell-line models. CCL22 expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, CCL22 is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, CCL22 RNA expression shows 12,646 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight HNSC, KIRC, and LSCC as cancer lineages where CCL22 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 CCL22 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CCL22 survival associations across molecular data types. CCL22 RNA expression shows survival associations in the most cancer types (28), followed by mutation status (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CCL22 RNA expression–survival associations across cancer types. High CCL22 expression shows unfavorable associations in ACC and UVM, but favorable associations in HNSC, UCEC, KIRC 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 CCL22 RNA expression.
This table summarizes CCL22 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for CCL22. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CCL22 shows lower tumor expression in KICH and higher tumor expression in KIRC, THCA, STAD, LUAD and CHOL. The KIRC box plot shows higher CCL22 RNA expression in tumor versus normal tissue (log2 FC = +0.868, t-test p < 0.001).
This table shows molecular features associated with CCL22 in patient tissues and cancer cell lines. In patient samples, CCL22 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, CCL22 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BLOOD_Leukemia.
