Q-omics provides the consensus-scored GRPR profile across patient tissues and cancer cell-line models. GRPR expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in BRCA. Among the 18 cancer types available for tumor–normal comparison, GRPR is differentially expressed in 10, with the highest sampling consensus in COAD. Additionally, GRPR RNA expression shows 18,091 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight BRCA, COAD, and UVM as cancer lineages where GRPR 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 GRPR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GRPR survival associations across molecular data types. GRPR 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 GRPR RNA expression–survival associations across cancer types. High GRPR expression shows unfavorable associations in LGG and MESO, but favorable associations in BRCA, KIRC, OV and SKCM. The BRCA 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 BRCA as the clearest survival context for GRPR RNA expression.
This table summarizes GRPR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 1. The strongest signals are observed in COAD for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for GRPR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GRPR shows lower tumor expression in STAD and higher tumor expression in COAD, KIRC, LIHC, KICH and UCEC. The COAD box plot shows higher GRPR RNA expression in tumor versus normal tissue (log2 FC = +0.921, t-test p < 0.001).
This table shows molecular features associated with GRPR in patient tissues and cancer cell lines. In patient samples, GRPR shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, GRPR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in CNS and LUNG_NSCLC_LUAD.
