Q-omics provides the consensus-scored GMPR profile across patient tissues and cancer cell-line models. GMPR expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, GMPR is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, GMPR protein abundance shows 20,797 significant protein co-abundance associations, with the highest sampling consensus in CCRCC. Together, these results highlight MESO, KIRC, and CCRCC as cancer lineages where GMPR 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 GMPR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GMPR survival associations across molecular data types. GMPR RNA expression shows survival associations in the most cancer types (22), followed by mutation status (1) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible GMPR RNA expression–survival associations across cancer types. High GMPR expression shows unfavorable associations in KIRP, LGG and SKCM, but favorable associations in MESO, OV and UCEC. The MESO 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 MESO as the clearest survival context for GMPR RNA expression.
This table summarizes GMPR 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 6. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for GMPR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GMPR shows lower tumor expression in KIRC, KIRP, LUSC and LUAD and higher tumor expression in COAD and THCA. The KIRC box plot shows higher GMPR RNA expression in normal versus tumor tissue (log2 FC = −2.490, t-test p < 0.001).
This table shows molecular features associated with GMPR in patient tissues and cancer cell lines. In patient samples, GMPR shows the broadest associations at the RNA and protein expression levels, with CCRCC recurring as the lineage with the largest associated feature set. In cancer cell lines, GMPR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in BONE and BLOOD_Leukemia.
