Q-omics provides the consensus-scored PXK profile across patient tissues and cancer cell-line models. PXK expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, PXK is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, PXK protein abundance shows 24,427 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight LUAD, KIRC, and LSCC as cancer lineages where PXK 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 PXK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PXK survival associations across molecular data types. PXK RNA expression shows survival associations in the most cancer types (22), followed by mutation status (6) 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 PXK RNA expression–survival associations across cancer types. High PXK expression shows unfavorable associations in LIHC, BLCA and CESC, but favorable associations in LUAD, HNSC and BRCA. The LUAD 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 LUAD as the clearest survival context for PXK RNA expression.
This table summarizes PXK tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PXK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PXK shows lower tumor expression in KIRC, THCA, LUSC, BLCA and LUAD and higher tumor expression in LIHC. The KIRC box plot shows higher PXK RNA expression in normal versus tumor tissue (log2 FC = −1.420, t-test p < 0.001).
This table shows molecular features associated with PXK in patient tissues and cancer cell lines. In patient samples, PXK 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, PXK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and BONE.
