ependymin related 1Genealiases: EPDR · MERP-1 · MERP1 · UCC1
Q-omics provides the consensus-scored EPDR1 profile across patient tissues and cancer cell-line models. EPDR1 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, EPDR1 is differentially expressed in 12, with the highest sampling consensus in KIRP. Additionally, EPDR1 protein abundance shows 21,425 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight UVM, KIRP, and HNSC as cancer lineages where EPDR1 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 EPDR1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes EPDR1 survival associations across molecular data types. EPDR1 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (4) 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 EPDR1 RNA expression–survival associations across cancer types. High EPDR1 expression shows unfavorable associations in UVM, STAD, BLCA, KIRP, LIHC and LGG. 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 EPDR1 RNA expression.
This table summarizes EPDR1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for EPDR1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. EPDR1 shows lower tumor expression in LUSC and UCEC and higher tumor expression in KIRP, KIRC, LIHC and KICH. The KIRP box plot shows higher EPDR1 RNA expression in tumor versus normal tissue (log2 FC = +1.541, t-test p < 0.001).
This table shows molecular features associated with EPDR1 in patient tissues and cancer cell lines. In patient samples, EPDR1 shows the broadest associations at the RNA and protein expression levels, with HNSC recurring as the lineage with the largest associated feature set. In cancer cell lines, EPDR1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and CNS.
