ENAH actin regulatorGenealiases: ENA · MENA · NDPP1
Q-omics provides the consensus-scored ENAH profile across patient tissues and cancer cell-line models. ENAH expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, ENAH is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, ENAH RNA expression shows 19,555 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight MESO, HNSC, and ACC as cancer lineages where ENAH 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 ENAH — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ENAH survival associations across molecular data types. ENAH RNA expression shows survival associations in the most cancer types (23), followed by mutation status (7) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ENAH RNA expression–survival associations across cancer types. High ENAH expression shows unfavorable associations in MESO, LIHC, KICH, ACC, BLCA and UVM. 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 ENAH RNA expression.
This table summarizes ENAH 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 4. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for ENAH. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ENAH shows lower tumor expression in KICH and higher tumor expression in HNSC, KIRP, LIHC, LUAD and BRCA. The HNSC box plot shows higher ENAH RNA expression in tumor versus normal tissue (log2 FC = +1.904, t-test p < 0.001).
This table shows molecular features associated with ENAH in patient tissues and cancer cell lines. In patient samples, ENAH shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, ENAH RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and BLOOD_Leukemia.
