Q-omics provides the consensus-scored ERO1A profile across patient tissues and cancer cell-line models. ERO1A expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, ERO1A is differentially expressed in 16, with the highest sampling consensus in KIRC. Additionally, ERO1A protein abundance shows 22,764 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, KIRC, and GBM as cancer lineages where ERO1A 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 ERO1A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ERO1A survival associations across molecular data types. ERO1A RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ERO1A RNA expression–survival associations across cancer types. High ERO1A expression shows unfavorable associations in KIRP, LUAD, MESO, LIHC, ACC and HNSC. The KIRP 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 KIRP as the clearest survival context for ERO1A RNA expression.
This table summarizes ERO1A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for ERO1A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ERO1A shows higher tumor expression in KIRC, LUAD, KIRP, THCA, LUSC and BLCA. The KIRC box plot shows higher ERO1A RNA expression in tumor versus normal tissue (log2 FC = +1.616, t-test p < 0.001).
This table shows molecular features associated with ERO1A in patient tissues and cancer cell lines. In patient samples, ERO1A 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, ERO1A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and BLOOD_Lymphoma.
