Q-omics provides the consensus-scored PNKD profile across patient tissues and cancer cell-line models. PNKD expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, PNKD is differentially expressed in 14, with the highest sampling consensus in KICH. Additionally, PNKD protein abundance shows 23,816 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight ACC, KICH, and LSCC as cancer lineages where PNKD 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 PNKD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PNKD survival associations across molecular data types. PNKD RNA expression shows survival associations in the most cancer types (27), followed by mutation status (3) 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 PNKD RNA expression–survival associations across cancer types. High PNKD expression shows unfavorable associations in ACC, KIRC, UCEC, SKCM and HNSC, but favorable associations in MESO. The ACC 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 ACC as the clearest survival context for PNKD RNA expression.
This table summarizes PNKD tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PNKD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PNKD shows lower tumor expression in KICH, KIRC and THCA and higher tumor expression in HNSC, LIHC and STAD. The KICH box plot shows higher PNKD RNA expression in normal versus tumor tissue (log2 FC = −1.991, t-test p < 0.001).
This table shows molecular features associated with PNKD in patient tissues and cancer cell lines. In patient samples, PNKD 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, PNKD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in CNS and BONE.
