Q-omics provides the consensus-scored CCL16 profile across patient tissues and cancer cell-line models. CCL16 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, CCL16 is differentially expressed in 12, with the highest sampling consensus in KIRP. Additionally, CCL16 RNA expression shows 14,123 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight MESO, KIRP, and LSCC as cancer lineages where CCL16 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 CCL16 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CCL16 survival associations across molecular data types. CCL16 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CCL16 RNA expression–survival associations across cancer types. High CCL16 expression shows unfavorable associations in MESO, KIRP and LUSC, but favorable associations in PAAD, READ and THCA. The MESO Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .004). Together, the overview and detailed table identify MESO as the clearest survival context for CCL16 RNA expression.
This table summarizes CCL16 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRP for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CCL16. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CCL16 shows lower tumor expression in KIRP, KICH, LUSC, BLCA, COAD and UCEC. The KIRP box plot shows higher CCL16 RNA expression in normal versus tumor tissue (log2 FC = −0.346, t-test p < 0.001).
This table shows molecular features associated with CCL16 in patient tissues and cancer cell lines. In patient samples, CCL16 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, CCL16 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 UPPER_AERODIGESTIVE_TRACT and SKIN.
