Q-omics provides the consensus-scored S1PR5 profile across patient tissues and cancer cell-line models. S1PR5 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, S1PR5 is differentially expressed in 11, with the highest sampling consensus in HNSC. Additionally, S1PR5 RNA expression shows 17,216 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, HNSC, and GBM as cancer lineages where S1PR5 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 S1PR5 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes S1PR5 survival associations across molecular data types. S1PR5 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible S1PR5 RNA expression–survival associations across cancer types. High S1PR5 expression shows unfavorable associations in KIRP, MESO, ACC, UVM and COAD, but favorable associations in HNSC. The KIRP 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 KIRP as the clearest survival context for S1PR5 RNA expression.
This table summarizes S1PR5 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for S1PR5. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. S1PR5 shows lower tumor expression in LUAD and higher tumor expression in HNSC, KIRC, COAD, BLCA and LUSC. The HNSC box plot shows higher S1PR5 RNA expression in tumor versus normal tissue (log2 FC = +1.728, t-test p < 0.001).
This table shows molecular features associated with S1PR5 in patient tissues and cancer cell lines. In patient samples, S1PR5 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, S1PR5 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and BONE.
