Q-omics provides the consensus-scored ESRRB profile across patient tissues and cancer cell-line models. ESRRB expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in THCA. Among the 18 cancer types available for tumor–normal comparison, ESRRB is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, ESRRB RNA expression shows 12,490 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight THCA, KIRC, and TGCT as cancer lineages where ESRRB 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 ESRRB — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ESRRB survival associations across molecular data types. ESRRB RNA expression shows survival associations in the most cancer types (26), followed by mutation status (5) 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 ESRRB RNA expression–survival associations across cancer types. High ESRRB expression shows unfavorable associations in THCA, THYM, LGG, UCEC and COAD, but favorable associations in KIRP. The THCA 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 THCA as the clearest survival context for ESRRB RNA expression.
This table summarizes ESRRB tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for ESRRB. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ESRRB shows lower tumor expression in KIRC, KIRP, KICH, BRCA, STAD and PAAD. The KIRC box plot shows higher ESRRB RNA expression in normal versus tumor tissue (log2 FC = −4.209, t-test p < 0.001).
This table shows molecular features associated with ESRRB in patient tissues and cancer cell lines. In patient samples, ESRRB shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, ESRRB RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BONE.
