Q-omics provides the consensus-scored EGLN3 profile across patient tissues and cancer cell-line models. EGLN3 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in DLBC. Among the 18 cancer types available for tumor–normal comparison, EGLN3 is differentially expressed in 16, with the highest sampling consensus in KIRC. Additionally, EGLN3 RNA expression shows 15,759 significant gene co-expression associations, with the highest sampling consensus in KIRC. Together, these results highlight DLBC, and KIRC as cancer lineages where EGLN3 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 EGLN3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes EGLN3 survival associations across molecular data types. EGLN3 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible EGLN3 RNA expression–survival associations across cancer types. High EGLN3 expression shows unfavorable associations in LIHC, LUAD, KICH and THCA, but favorable associations in DLBC and KIRC. The DLBC 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 DLBC as the clearest survival context for EGLN3 RNA expression.
This table summarizes EGLN3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for EGLN3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. EGLN3 shows lower tumor expression in KICH and higher tumor expression in KIRC, LUAD, LUSC, HNSC and LIHC. The KIRC box plot shows higher EGLN3 RNA expression in tumor versus normal tissue (log2 FC = +4.508, t-test p < 0.001).
This table shows molecular features associated with EGLN3 in patient tissues and cancer cell lines. In patient samples, EGLN3 shows the broadest associations at the RNA and protein expression levels, with KIRC recurring as the lineage with the largest associated feature set. In cancer cell lines, EGLN3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and OVARY.
