Q-omics provides the consensus-scored EPM2A profile across patient tissues and cancer cell-line models. EPM2A expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, EPM2A is differentially expressed in 16, with the highest sampling consensus in KIRC. Additionally, EPM2A protein abundance shows 24,670 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, and GBM as cancer lineages where EPM2A 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 EPM2A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes EPM2A survival associations across molecular data types. EPM2A RNA expression shows survival associations in the most cancer types (19), followed by mutation status (2) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible EPM2A RNA expression–survival associations across cancer types. High EPM2A expression shows favorable associations in KIRC, PAAD, GBM, UVM, LIHC and KIRP. 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 EPM2A RNA expression.
This table summarizes EPM2A 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 6. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for EPM2A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. EPM2A shows lower tumor expression in KIRC, KIRP, THCA, KICH, LUAD and BLCA. The KIRC box plot shows higher EPM2A RNA expression in normal versus tumor tissue (log2 FC = −1.137, t-test p < 0.001).
This table shows molecular features associated with EPM2A in patient tissues and cancer cell lines. In patient samples, EPM2A 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, EPM2A 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 BONE and BLOOD_Leukemia.
