Q-omics provides the consensus-scored PEX3 profile across patient tissues and cancer cell-line models. PEX3 expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in OV. Among the 18 cancer types available for tumor–normal comparison, PEX3 is differentially expressed in 12, with the highest sampling consensus in KICH. Additionally, PEX3 protein abundance shows 37,207 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight OV, KICH, and LUAD as cancer lineages where PEX3 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 PEX3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PEX3 survival associations across molecular data types. PEX3 RNA expression shows survival associations in the most cancer types (19), followed by mutation status (4) and mass-spec protein abundance (13). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PEX3 RNA expression–survival associations across cancer types. High PEX3 expression shows unfavorable associations in OV, BLCA and LIHC, but favorable associations in KIRC, READ and ACC. The OV 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 OV as the clearest survival context for PEX3 RNA expression.
This table summarizes PEX3 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 12. The strongest signals are observed in KICH for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for PEX3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PEX3 shows lower tumor expression in KICH, THCA, KIRC, KIRP and LUAD and higher tumor expression in COAD. The KICH box plot shows higher PEX3 RNA expression in normal versus tumor tissue (log2 FC = −2.134, t-test p < 0.001).
This table shows molecular features associated with PEX3 in patient tissues and cancer cell lines. In patient samples, PEX3 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, PEX3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and CNS.
