Q-omics provides the consensus-scored PEX6 profile across patient tissues and cancer cell-line models. PEX6 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in THYM. Among the 18 cancer types available for tumor–normal comparison, PEX6 is differentially expressed in 9, with the highest sampling consensus in LIHC. Additionally, PEX6 protein abundance shows 26,045 significant protein co-abundance associations, with the highest sampling consensus in CCRCC. Together, these results highlight THYM, LIHC, and CCRCC as cancer lineages where PEX6 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 PEX6 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PEX6 survival associations across molecular data types. PEX6 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (7) and mass-spec protein abundance (11). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PEX6 RNA expression–survival associations across cancer types. High PEX6 expression shows unfavorable associations in KIRC, LUAD, SARC, UCS and MESO, but favorable associations in THYM. The THYM Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .002). Together, the overview and detailed table identify THYM as the clearest survival context for PEX6 RNA expression.
This table summarizes PEX6 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 9. The strongest signals are observed in LIHC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PEX6. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PEX6 shows lower tumor expression in KICH and UCEC and higher tumor expression in LIHC, CHOL, COAD and PRAD. The LIHC box plot shows higher PEX6 RNA expression in tumor versus normal tissue (log2 FC = +1.224, t-test p < 0.001).
This table shows molecular features associated with PEX6 in patient tissues and cancer cell lines. In patient samples, PEX6 shows the broadest associations at the RNA and protein expression levels, with CCRCC recurring as the lineage with the largest associated feature set. In cancer cell lines, PEX6 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LARGE_INTESTINE.
