Q-omics provides the consensus-scored PEX11G profile across patient tissues and cancer cell-line models. PEX11G expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PEX11G is differentially expressed in 9, with the highest sampling consensus in LUAD. Additionally, PEX11G protein abundance shows 22,852 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, LUAD, and LSCC as cancer lineages where PEX11G 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 PEX11G — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PEX11G survival associations across molecular data types. PEX11G RNA expression shows survival associations in the most cancer types (26), followed by mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PEX11G RNA expression–survival associations across cancer types. High PEX11G expression shows unfavorable associations in LGG, but favorable associations in KIRC, KIRP, UCEC, BRCA and LIHC. 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 PEX11G RNA expression.
This table summarizes PEX11G 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 7. The strongest signals are observed in LUAD for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for PEX11G. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PEX11G shows lower tumor expression in LUAD, KICH, LIHC, THCA, KIRC and CHOL. The LUAD box plot shows higher PEX11G RNA expression in normal versus tumor tissue (log2 FC = −0.732, t-test p < 0.001).
This table shows molecular features associated with PEX11G in patient tissues and cancer cell lines. In patient samples, PEX11G shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, PEX11G RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in BREAST and SOFT_TISSUE.
