Q-omics provides the consensus-scored ESRRG profile across patient tissues and cancer cell-line models. ESRRG expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, ESRRG is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, ESRRG RNA expression shows 17,207 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight KIRC, and KIRP as cancer lineages where ESRRG 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 ESRRG — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ESRRG survival associations across molecular data types. ESRRG RNA expression shows survival associations in the most cancer types (25), followed by mutation status (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ESRRG RNA expression–survival associations across cancer types. High ESRRG expression shows unfavorable associations in ACC, but favorable associations in KIRC, UVM, SCLC, MESO and PRAD. 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 ESRRG RNA expression.
This table summarizes ESRRG 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 CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for ESRRG. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ESRRG shows lower tumor expression in KIRC, KIRP, THCA, STAD, HNSC and KICH. The KIRC box plot shows higher ESRRG RNA expression in normal versus tumor tissue (log2 FC = −3.193, t-test p < 0.001).
This table shows molecular features associated with ESRRG in patient tissues and cancer cell lines. In patient samples, ESRRG shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, ESRRG RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and OVARY.
