Q-omics provides the consensus-scored CXCR2 profile across patient tissues and cancer cell-line models. CXCR2 expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, CXCR2 is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, CXCR2 RNA expression shows 20,816 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight MESO, HNSC, and LSCC as cancer lineages where CXCR2 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 CXCR2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CXCR2 survival associations across molecular data types. CXCR2 RNA expression shows survival associations in the most cancer types (28), followed by mutation status (9) 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 CXCR2 RNA expression–survival associations across cancer types. High CXCR2 expression shows unfavorable associations in LAML, LGG and OV, but favorable associations in MESO, UCEC and KIRC. The MESO Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .002). Together, the overview and detailed table identify MESO as the clearest survival context for CXCR2 RNA expression.
This table summarizes CXCR2 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 2. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CXCR2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CXCR2 shows lower tumor expression in HNSC, LUAD, LUSC, BRCA and LIHC and higher tumor expression in KIRC. The HNSC box plot shows higher CXCR2 RNA expression in normal versus tumor tissue (log2 FC = −3.043, t-test p < 0.001).
This table shows molecular features associated with CXCR2 in patient tissues and cancer cell lines. In patient samples, CXCR2 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, CXCR2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BLOOD_Leukemia.
