Q-omics provides the consensus-scored PNKP profile across patient tissues and cancer cell-line models. PNKP expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, PNKP is differentially expressed in 15, with the highest sampling consensus in COAD. Additionally, PNKP protein abundance shows 24,807 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight UVM, COAD, and GBM as cancer lineages where PNKP 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 PNKP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PNKP survival associations across molecular data types. PNKP RNA expression shows survival associations in the most cancer types (21), followed by mutation status (4) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PNKP RNA expression–survival associations across cancer types. High PNKP expression shows unfavorable associations in UVM, KIRC, ACC, LGG, SKCM 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 PNKP RNA expression.
This table summarizes PNKP tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 10. The strongest signals are observed in KIRP for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for PNKP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PNKP shows higher tumor expression in COAD, KIRP, BLCA, HNSC, LIHC and LUAD. The COAD box plot shows higher PNKP RNA expression in tumor versus normal tissue (log2 FC = +0.987, t-test p < 0.001).
This table shows molecular features associated with PNKP in patient tissues and cancer cell lines. In patient samples, PNKP shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, PNKP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and BLOOD_Leukemia.
