Q-omics provides the consensus-scored ELN profile across patient tissues and cancer cell-line models. ELN expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, ELN is differentially expressed in 11, with the highest sampling consensus in KICH. Additionally, ELN protein abundance shows 32,429 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRP, KICH, and LUAD as cancer lineages where ELN 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 ELN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ELN survival associations across molecular data types. ELN RNA expression shows survival associations in the most cancer types (28), followed by mutation status (3) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ELN RNA expression–survival associations across cancer types. High ELN expression shows unfavorable associations in KIRP, BLCA and LGG, but favorable associations in HNSC, KIRC and UCS. 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 ELN RNA expression.
This table summarizes ELN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 10. The strongest signals are observed in KICH for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for ELN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ELN shows lower tumor expression in KICH, BLCA, LUAD, LUSC and UCEC and higher tumor expression in COAD. The KICH box plot shows higher ELN RNA expression in normal versus tumor tissue (log2 FC = −1.996, t-test p < 0.001).
This table shows molecular features associated with ELN in patient tissues and cancer cell lines. In patient samples, ELN shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, ELN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BONE.
