Q-omics provides the consensus-scored CCR2 profile across patient tissues and cancer cell-line models. CCR2 expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, CCR2 is differentially expressed in 7, with the highest sampling consensus in KIRC. Additionally, CCR2 RNA expression shows 22,630 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight SKCM, KIRC, and LSCC as cancer lineages where CCR2 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 CCR2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CCR2 survival associations across molecular data types. CCR2 RNA expression shows survival associations in the most cancer types (28), followed by mutation status (4) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CCR2 RNA expression–survival associations across cancer types. High CCR2 expression shows unfavorable associations in LGG, but favorable associations in SKCM, HNSC, LUAD, CESC and UCS. 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 CCR2 RNA expression.
This table summarizes CCR2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 7, while mass-spec protein shows differences in 4. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for CCR2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CCR2 shows lower tumor expression in COAD, LUSC, UCEC, KICH and READ and higher tumor expression in KIRC. The KIRC box plot shows higher CCR2 RNA expression in tumor versus normal tissue (log2 FC = +1.672, t-test p < 0.001).
This table shows molecular features associated with CCR2 in patient tissues and cancer cell lines. In patient samples, CCR2 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, CCR2 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 CNS and BLOOD_Leukemia.
