Q-omics provides the consensus-scored GPRACR profile across patient tissues and cancer cell-line models. GPRACR expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, GPRACR is differentially expressed in 11, with the highest sampling consensus in HNSC. Additionally, GPRACR RNA expression shows 11,901 significant gene co-expression associations, with the highest sampling consensus in PAAD. Together, these results highlight KIRC, HNSC, and PAAD as cancer lineages where GPRACR 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 GPRACR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GPRACR survival associations across molecular data types. GPRACR RNA expression shows survival associations in the most cancer types (26). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible GPRACR RNA expression–survival associations across cancer types. High GPRACR expression shows unfavorable associations in KIRC, CESC, ACC, LGG and UVM, but favorable associations in KIRP. 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 GPRACR RNA expression.
This table summarizes GPRACR 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 HNSC for RNA.
This table ranks reproducible tumor–normal expression differences for GPRACR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GPRACR shows lower tumor expression in THCA, READ and COAD and higher tumor expression in HNSC, LUAD and BRCA. The HNSC box plot shows higher GPRACR RNA expression in tumor versus normal tissue (log2 FC = +0.257, t-test p < 0.001).
This table shows molecular features associated with GPRACR in patient tissues and cancer cell lines. In patient samples, GPRACR shows the broadest associations at the RNA and protein expression levels, with PAAD recurring as the lineage with the largest associated feature set.