Q-omics provides the consensus-scored PDXK profile across patient tissues and cancer cell-line models. PDXK expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, PDXK is differentially expressed in 13, with the highest sampling consensus in BLCA. Additionally, PDXK protein abundance shows 28,244 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight UVM, BLCA, and LSCC as cancer lineages where PDXK 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 PDXK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PDXK survival associations across molecular data types. PDXK RNA expression shows survival associations in the most cancer types (28), followed by mutation status (7) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PDXK RNA expression–survival associations across cancer types. High PDXK expression shows unfavorable associations in UVM, BRCA, LUAD, CESC, KIRC and LIHC. The UVM 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 UVM as the clearest survival context for PDXK RNA expression.
This table summarizes PDXK 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 4. The strongest signals are observed in BLCA for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for PDXK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PDXK shows lower tumor expression in KIRC and KICH and higher tumor expression in BLCA, LIHC, STAD and COAD. The BLCA box plot shows higher PDXK RNA expression in tumor versus normal tissue (log2 FC = +1.498, t-test p < 0.001).
This table shows molecular features associated with PDXK in patient tissues and cancer cell lines. In patient samples, PDXK 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, PDXK 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 OVARY and CNS.
