Q-omics provides the consensus-scored HNF4A profile across patient tissues and cancer cell-line models. HNF4A expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, HNF4A is differentially expressed in 10, with the highest sampling consensus in KICH. Additionally, HNF4A protein abundance shows 22,107 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, KICH, and GBM as cancer lineages where HNF4A 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 HNF4A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HNF4A survival associations across molecular data types. HNF4A RNA expression shows survival associations in the most cancer types (24), followed by mutation status (10) 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 HNF4A RNA expression–survival associations across cancer types. High HNF4A expression shows unfavorable associations in KICH, THCA, DLBC and CHOL, but favorable associations in KIRP and KIRC. The KIRP 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 KIRP as the clearest survival context for HNF4A RNA expression.
This table summarizes HNF4A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 9. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for HNF4A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HNF4A shows lower tumor expression in KICH and KIRP and higher tumor expression in HNSC, STAD, LUAD and LIHC. The KICH box plot shows higher HNF4A RNA expression in normal versus tumor tissue (log2 FC = −3.738, t-test p < 0.001).
This table shows molecular features associated with HNF4A in patient tissues and cancer cell lines. In patient samples, HNF4A 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, HNF4A 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 SOFT_TISSUE and BLOOD_Lymphoma.
