Q-omics provides the consensus-scored CCL7 profile across patient tissues and cancer cell-line models. CCL7 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CCL7 is differentially expressed in 9, with the highest sampling consensus in HNSC. Additionally, CCL7 RNA expression shows 18,657 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, HNSC, and GBM as cancer lineages where CCL7 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 CCL7 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CCL7 survival associations across molecular data types. CCL7 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (4) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CCL7 RNA expression–survival associations across cancer types. High CCL7 expression shows unfavorable associations in KIRC, LAML and KICH, but favorable associations in SKCM, MESO and OV. The KIRC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for CCL7 RNA expression.
This table summarizes CCL7 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 4. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CCL7. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CCL7 shows lower tumor expression in KICH and higher tumor expression in HNSC, THCA, LUAD, STAD and BRCA. The HNSC box plot shows higher CCL7 RNA expression in tumor versus normal tissue (log2 FC = +0.870, t-test p < 0.001).
This table shows molecular features associated with CCL7 in patient tissues and cancer cell lines. In patient samples, CCL7 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, CCL7 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 CNS and SKIN.
