Q-omics provides the consensus-scored EPPIN profile across patient tissues and cancer cell-line models. EPPIN expression is associated with patient survival in 18 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, EPPIN is differentially expressed in 10, with the highest sampling consensus in LUAD. Additionally, EPPIN RNA expression shows 10,415 significant gene co-expression associations, with the highest sampling consensus in SCLC. Together, these results highlight KIRC, LUAD, and SCLC as cancer lineages where EPPIN 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 EPPIN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes EPPIN survival associations across molecular data types. EPPIN RNA expression shows survival associations in the most cancer types (18), followed by mutation status (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible EPPIN RNA expression–survival associations across cancer types. High EPPIN expression shows unfavorable associations in KIRC, COAD, LIHC and THCA, but favorable associations in HNSC and UCEC. The KIRC 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 KIRC as the clearest survival context for EPPIN RNA expression.
This table summarizes EPPIN 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 LUAD for RNA.
This table ranks reproducible tumor–normal expression differences for EPPIN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. EPPIN shows lower tumor expression in LUAD, LUSC, THCA, BRCA, KICH and KIRC. The LUAD box plot shows higher EPPIN RNA expression in normal versus tumor tissue (log2 FC = −0.322, t-test p < 0.001).
This table shows molecular features associated with EPPIN in patient tissues and cancer cell lines. In patient samples, EPPIN shows the broadest associations at the RNA and protein expression levels, with SCLC recurring as the lineage with the largest associated feature set. In cancer cell lines, EPPIN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in OVARY and LUNG_SCLC.
