Q-omics provides the consensus-scored PNCK profile across patient tissues and cancer cell-line models. PNCK expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in LIHC. Among the 18 cancer types available for tumor–normal comparison, PNCK is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, PNCK RNA expression shows 16,754 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight LIHC, KIRC, and GBM as cancer lineages where PNCK 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 PNCK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PNCK survival associations across molecular data types. PNCK RNA expression shows survival associations in the most cancer types (24), followed by mutation status (6) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PNCK RNA expression–survival associations across cancer types. High PNCK expression shows unfavorable associations in LIHC, ACC, UCEC, UCS and KICH, but favorable associations in OV. The LIHC 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 LIHC as the clearest survival context for PNCK RNA expression.
This table summarizes PNCK 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 1. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PNCK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PNCK shows lower tumor expression in STAD and COAD and higher tumor expression in KIRC, HNSC, LUSC and LUAD. The KIRC box plot shows higher PNCK RNA expression in tumor versus normal tissue (log2 FC = +4.652, t-test p < 0.001).
This table shows molecular features associated with PNCK in patient tissues and cancer cell lines. In patient samples, PNCK 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, PNCK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BONE.
