Q-omics provides the consensus-scored EPHA3 profile across patient tissues and cancer cell-line models. EPHA3 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, EPHA3 is differentially expressed in 10, with the highest sampling consensus in THCA. Additionally, EPHA3 RNA expression shows 17,379 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRP, THCA, and PDAC as cancer lineages where EPHA3 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 EPHA3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes EPHA3 survival associations across molecular data types. EPHA3 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (9) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible EPHA3 RNA expression–survival associations across cancer types. High EPHA3 expression shows unfavorable associations in KIRP, ACC, BLCA, UVM and BRCA, but favorable associations in 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 EPHA3 RNA expression.
This table summarizes EPHA3 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 1. The strongest signals are observed in THCA for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for EPHA3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. EPHA3 shows lower tumor expression in THCA, BLCA, KICH, LUSC and COAD and higher tumor expression in KIRC. The THCA box plot shows higher EPHA3 RNA expression in normal versus tumor tissue (log2 FC = −2.787, t-test p < 0.001).
This table shows molecular features associated with EPHA3 in patient tissues and cancer cell lines. In patient samples, EPHA3 shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, EPHA3 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 LARGE_INTESTINE and BONE.
