Q-omics provides the consensus-scored GRM3 profile across patient tissues and cancer cell-line models. GRM3 expression is associated with patient survival in 18 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, GRM3 is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, GRM3 RNA expression shows 17,242 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight HNSC, KIRC, and GBM as cancer lineages where GRM3 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 GRM3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GRM3 survival associations across molecular data types. GRM3 RNA expression shows survival associations in the most cancer types (18), followed by mutation status (13) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible GRM3 RNA expression–survival associations across cancer types. High GRM3 expression shows unfavorable associations in HNSC, LUSC and STAD, but favorable associations in SCLC, OV and KIRC. The HNSC 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 HNSC as the clearest survival context for GRM3 RNA expression.
This table summarizes GRM3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for GRM3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GRM3 shows lower tumor expression in KIRC, KIRP, LUAD, LUSC and KICH and higher tumor expression in HNSC. The KIRC box plot shows higher GRM3 RNA expression in normal versus tumor tissue (log2 FC = −0.316, t-test p < 0.001).
This table shows molecular features associated with GRM3 in patient tissues and cancer cell lines. In patient samples, GRM3 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, GRM3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and LARGE_INTESTINE.
