Q-omics provides the consensus-scored HNF4G profile across patient tissues and cancer cell-line models. HNF4G expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, HNF4G is differentially expressed in 9, with the highest sampling consensus in KIRC. Additionally, HNF4G RNA expression shows 16,896 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight KIRC, and THYM as cancer lineages where HNF4G 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 HNF4G — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HNF4G survival associations across molecular data types. HNF4G RNA expression shows survival associations in the most cancer types (24), followed by mutation status (3) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible HNF4G RNA expression–survival associations across cancer types. High HNF4G expression shows unfavorable associations in ACC, MESO, LUAD and LGG, but favorable associations in KIRC and SKCM. 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 HNF4G RNA expression.
This table summarizes HNF4G 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 2. The strongest signals are observed in KIRC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for HNF4G. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HNF4G shows lower tumor expression in KICH and COAD and higher tumor expression in KIRC, LUAD, STAD and LUSC. The KIRC box plot shows higher HNF4G RNA expression in tumor versus normal tissue (log2 FC = +1.448, t-test p < 0.001).
This table shows molecular features associated with HNF4G in patient tissues and cancer cell lines. In patient samples, HNF4G shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, HNF4G RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BONE.