Q-omics provides the consensus-scored EML1 profile across patient tissues and cancer cell-line models. EML1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, EML1 is differentially expressed in 15, with the highest sampling consensus in THCA. Additionally, EML1 protein abundance shows 27,656 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRC, THCA, and LUAD as cancer lineages where EML1 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 EML1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes EML1 survival associations across molecular data types. EML1 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (7) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible EML1 RNA expression–survival associations across cancer types. High EML1 expression shows unfavorable associations in BLCA, STAD and COAD, but favorable associations in KIRC, OV and ACC. 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 EML1 RNA expression.
This table summarizes EML1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 7. The strongest signals are observed in THCA for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for EML1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. EML1 shows lower tumor expression in THCA, LUAD, KICH, COAD and BLCA and higher tumor expression in HNSC. The THCA box plot shows higher EML1 RNA expression in normal versus tumor tissue (log2 FC = −1.884, t-test p < 0.001).
This table shows molecular features associated with EML1 in patient tissues and cancer cell lines. In patient samples, EML1 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, EML1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in LIVER and BLOOD_Lymphoma.
