Q-omics provides the consensus-scored EMCN profile across patient tissues and cancer cell-line models. EMCN expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, EMCN is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, EMCN RNA expression shows 23,543 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, and LSCC as cancer lineages where EMCN 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 EMCN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes EMCN survival associations across molecular data types. EMCN RNA expression shows survival associations in the most cancer types (24), followed by mutation status (2) 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 EMCN RNA expression–survival associations across cancer types. High EMCN expression shows unfavorable associations in KIRP and MESO, but favorable associations in KIRC, LIHC, KICH and THCA. 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 EMCN RNA expression.
This table summarizes EMCN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for EMCN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. EMCN shows lower tumor expression in KIRC, KICH, KIRP, BLCA, THCA and LUSC. The KIRC box plot shows higher EMCN RNA expression in normal versus tumor tissue (log2 FC = −1.537, t-test p < 0.001).
This table shows molecular features associated with EMCN in patient tissues and cancer cell lines. In patient samples, EMCN shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, EMCN 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 BLOOD_Leukemia and LARGE_INTESTINE.
