Q-omics provides the consensus-scored PEX5 profile across patient tissues and cancer cell-line models. PEX5 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in STAD. Among the 18 cancer types available for tumor–normal comparison, PEX5 is differentially expressed in 14, with the highest sampling consensus in COAD. Additionally, PEX5 RNA expression shows 19,456 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight STAD, COAD, and ACC as cancer lineages where PEX5 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 PEX5 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PEX5 survival associations across molecular data types. PEX5 RNA expression shows survival associations in the most cancer types (22), 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 PEX5 RNA expression–survival associations across cancer types. High PEX5 expression shows unfavorable associations in COAD, ACC and CESC, but favorable associations in STAD, KIRC and READ. The STAD 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 STAD as the clearest survival context for PEX5 RNA expression.
This table summarizes PEX5 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 7. The strongest signals are observed in COAD for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for PEX5. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PEX5 shows lower tumor expression in LUAD and THCA and higher tumor expression in COAD, LIHC, HNSC and KIRC. The COAD box plot shows higher PEX5 RNA expression in tumor versus normal tissue (log2 FC = +0.894, t-test p < 0.001).
This table shows molecular features associated with PEX5 in patient tissues and cancer cell lines. In patient samples, PEX5 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, PEX5 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 BLOOD_Lymphoma.