Q-omics provides the consensus-scored EMILIN3 profile across patient tissues and cancer cell-line models. EMILIN3 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, EMILIN3 is differentially expressed in 15, with the highest sampling consensus in COAD. Additionally, EMILIN3 RNA expression shows 16,615 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight UVM, COAD, and TGCT as cancer lineages where EMILIN3 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 EMILIN3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes EMILIN3 survival associations across molecular data types. EMILIN3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (6) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible EMILIN3 RNA expression–survival associations across cancer types. High EMILIN3 expression shows unfavorable associations in UVM, LGG, STAD and ACC, but favorable associations in UCS and BRCA. 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 EMILIN3 RNA expression.
This table summarizes EMILIN3 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 3. The strongest signals are observed in KIRP for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for EMILIN3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. EMILIN3 shows lower tumor expression in COAD, KIRP, STAD, KIRC, KICH and UCEC. The COAD box plot shows higher EMILIN3 RNA expression in normal versus tumor tissue (log2 FC = −1.005, t-test p < 0.001).
This table shows molecular features associated with EMILIN3 in patient tissues and cancer cell lines. In patient samples, EMILIN3 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, EMILIN3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and BONE.
