Q-omics provides the consensus-scored GRIK2 profile across patient tissues and cancer cell-line models. GRIK2 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in STAD. Among the 18 cancer types available for tumor–normal comparison, GRIK2 is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, GRIK2 RNA expression shows 15,416 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight STAD, KIRC, and UVM as cancer lineages where GRIK2 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 GRIK2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GRIK2 survival associations across molecular data types. GRIK2 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (8) 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 GRIK2 RNA expression–survival associations across cancer types. High GRIK2 expression shows unfavorable associations in STAD, LUAD, BLCA, SKCM and COAD, but favorable associations in LGG. The STAD Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .003). Together, the overview and detailed table identify STAD as the clearest survival context for GRIK2 RNA expression.
This table summarizes GRIK2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for GRIK2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GRIK2 shows lower tumor expression in KIRC, KIRP, KICH, THCA and COAD and higher tumor expression in LUAD. The KIRC box plot shows higher GRIK2 RNA expression in normal versus tumor tissue (log2 FC = −1.010, t-test p < 0.001).
This table shows molecular features associated with GRIK2 in patient tissues and cancer cell lines. In patient samples, GRIK2 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, GRIK2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in LIVER and LARGE_INTESTINE.
