Q-omics provides the consensus-scored EPOR profile across patient tissues and cancer cell-line models. EPOR expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, EPOR is differentially expressed in 10, with the highest sampling consensus in HNSC. Additionally, EPOR RNA expression shows 18,150 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight MESO, HNSC, and UVM as cancer lineages where EPOR 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 EPOR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes EPOR survival associations across molecular data types. EPOR RNA expression shows survival associations in the most cancer types (26), followed by mutation status (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible EPOR RNA expression–survival associations across cancer types. High EPOR expression shows unfavorable associations in MESO, KIRP, LUSC, KIRC and PRAD, but favorable associations in BLCA. The MESO 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 MESO as the clearest survival context for EPOR RNA expression.
This table summarizes EPOR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10. The strongest signals are observed in HNSC for RNA.
This table ranks reproducible tumor–normal expression differences for EPOR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. EPOR shows lower tumor expression in LUSC and LUAD and higher tumor expression in HNSC, UCEC, COAD and THCA. The HNSC box plot shows higher EPOR RNA expression in tumor versus normal tissue (log2 FC = +1.066, t-test p < 0.001).
This table shows molecular features associated with EPOR in patient tissues and cancer cell lines. In patient samples, EPOR shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, EPOR 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 OVARY and LARGE_INTESTINE.
