Q-omics provides the consensus-scored EDIL3 profile across patient tissues and cancer cell-line models. EDIL3 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, EDIL3 is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, EDIL3 RNA expression shows 21,500 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight UVM, HNSC, and GBM as cancer lineages where EDIL3 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 EDIL3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes EDIL3 survival associations across molecular data types. EDIL3 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (9) 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 EDIL3 RNA expression–survival associations across cancer types. High EDIL3 expression shows unfavorable associations in UVM, MESO, BLCA, ACC and STAD, but favorable associations in LUAD. The UVM 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 UVM as the clearest survival context for EDIL3 RNA expression.
This table summarizes EDIL3 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 5. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for EDIL3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. EDIL3 shows lower tumor expression in KICH, COAD and LUSC and higher tumor expression in HNSC, LIHC and KIRC. The HNSC box plot shows higher EDIL3 RNA expression in tumor versus normal tissue (log2 FC = +2.114, t-test p < 0.001).
This table shows molecular features associated with EDIL3 in patient tissues and cancer cell lines. In patient samples, EDIL3 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, EDIL3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and SOFT_TISSUE.
