Q-omics provides the consensus-scored FPR3 profile across patient tissues and cancer cell-line models. FPR3 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, FPR3 is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, FPR3 RNA expression shows 22,104 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight SKCM, KIRC, and LSCC as cancer lineages where FPR3 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 FPR3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FPR3 survival associations across molecular data types. FPR3 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FPR3 RNA expression–survival associations across cancer types. High FPR3 expression shows unfavorable associations in UVM, but favorable associations in SKCM, KIRC, HNSC, DLBC and LUAD. 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 FPR3 RNA expression.
This table summarizes FPR3 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 1. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for FPR3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FPR3 shows higher tumor expression in KIRC, HNSC, STAD, BRCA, KIRP and THCA. The KIRC box plot shows higher FPR3 RNA expression in tumor versus normal tissue (log2 FC = +2.832, t-test p < 0.001).
This table shows molecular features associated with FPR3 in patient tissues and cancer cell lines. In patient samples, FPR3 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, FPR3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and LARGE_INTESTINE.
