Q-omics provides the consensus-scored PEX1 profile across patient tissues and cancer cell-line models. PEX1 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PEX1 is differentially expressed in 13, with the highest sampling consensus in THCA. Additionally, PEX1 protein abundance shows 32,490 significant protein co-abundance associations, with the highest sampling consensus in UCEC. Together, these results highlight KIRC, THCA, and UCEC as cancer lineages where PEX1 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 PEX1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PEX1 survival associations across molecular data types. PEX1 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (7) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PEX1 RNA expression–survival associations across cancer types. High PEX1 expression shows unfavorable associations in LGG and KICH, but favorable associations in KIRC, HNSC, LAML and UCS. The KIRC 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 KIRC as the clearest survival context for PEX1 RNA expression.
This table summarizes PEX1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 9. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PEX1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PEX1 shows lower tumor expression in THCA, KIRP, KIRC and KICH and higher tumor expression in LIHC and CHOL. The THCA box plot shows higher PEX1 RNA expression in normal versus tumor tissue (log2 FC = −0.694, t-test p < 0.001).
This table shows molecular features associated with PEX1 in patient tissues and cancer cell lines. In patient samples, PEX1 shows the broadest associations at the RNA and protein expression levels, with UCEC recurring as the lineage with the largest associated feature set. In cancer cell lines, PEX1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LARGE_INTESTINE.
