Q-omics provides the consensus-scored GRHL2 profile across patient tissues and cancer cell-line models. GRHL2 expression is associated with patient survival in 15 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, GRHL2 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, GRHL2 protein abundance shows 29,580 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, and LSCC as cancer lineages where GRHL2 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 GRHL2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GRHL2 survival associations across molecular data types. GRHL2 RNA expression shows survival associations in the most cancer types (15), followed by mutation status (5) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible GRHL2 RNA expression–survival associations across cancer types. High GRHL2 expression shows unfavorable associations in KIRC, SKCM, PAAD and BRCA, but favorable associations in BLCA and STAD. The KIRC 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 KIRC as the clearest survival context for GRHL2 RNA expression.
This table summarizes GRHL2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 8. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for GRHL2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GRHL2 shows lower tumor expression in KIRC and KIRP and higher tumor expression in BLCA, COAD, LUSC and LUAD. The KIRC box plot shows higher GRHL2 RNA expression in normal versus tumor tissue (log2 FC = −3.530, t-test p < 0.001).
This table shows molecular features associated with GRHL2 in patient tissues and cancer cell lines. In patient samples, GRHL2 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, GRHL2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BLOOD_Leukemia.
