glyoxylate and hydroxypyruvate reductaseGenealiases: GLXR · GLYD · PH2
Q-omics provides the consensus-scored GRHPR profile across patient tissues and cancer cell-line models. GRHPR expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, GRHPR is differentially expressed in 9, with the highest sampling consensus in KIRP. Additionally, GRHPR protein abundance shows 22,049 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRC, KIRP, and PDAC as cancer lineages where GRHPR 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 GRHPR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GRHPR survival associations across molecular data types. GRHPR RNA expression shows survival associations in the most cancer types (21), followed by mutation status (8) 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 GRHPR RNA expression–survival associations across cancer types. High GRHPR expression shows unfavorable associations in ACC and UVM, but favorable associations in KIRC, KIRP, GBM and BRCA. The KIRC 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 KIRC as the clearest survival context for GRHPR RNA expression.
This table summarizes GRHPR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRP for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for GRHPR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GRHPR shows lower tumor expression in KIRP, KICH, KIRC, CHOL and LIHC and higher tumor expression in COAD. The KIRP box plot shows higher GRHPR RNA expression in normal versus tumor tissue (log2 FC = −0.904, t-test p < 0.001).
This table shows molecular features associated with GRHPR in patient tissues and cancer cell lines. In patient samples, GRHPR shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, GRHPR 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 BONE and SOFT_TISSUE.
