Q-omics provides the consensus-scored GRN profile across patient tissues and cancer cell-line models. GRN expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, GRN is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, GRN RNA expression shows 18,062 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRP, KIRC, and ACC as cancer lineages where GRN 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 GRN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GRN survival associations across molecular data types. GRN RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) 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 GRN RNA expression–survival associations across cancer types. High GRN expression shows unfavorable associations in KIRP, LGG, HNSC, BLCA and LIHC, but favorable associations in KIRC. The KIRP Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify KIRP as the clearest survival context for GRN RNA expression.
This table summarizes GRN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for GRN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GRN shows lower tumor expression in LUAD and higher tumor expression in KIRC, KIRP, LIHC, HNSC and STAD. The KIRC box plot shows higher GRN RNA expression in tumor versus normal tissue (log2 FC = +0.875, t-test p < 0.001).
This table shows molecular features associated with GRN in patient tissues and cancer cell lines. In patient samples, GRN shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, GRN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BONE.
