Q-omics provides the consensus-scored PNMT profile across patient tissues and cancer cell-line models. PNMT expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KICH. Among the 18 cancer types available for tumor–normal comparison, PNMT is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, PNMT RNA expression shows 13,030 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight KICH, KIRC, and THYM as cancer lineages where PNMT 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 PNMT — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PNMT survival associations across molecular data types. PNMT RNA expression shows survival associations in the most cancer types (21), followed by mutation status (3) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PNMT RNA expression–survival associations across cancer types. High PNMT expression shows unfavorable associations in MESO, LGG and KIRP, but favorable associations in KICH, LUAD and LUSC. The KICH Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .013). Together, the overview and detailed table identify KICH as the clearest survival context for PNMT RNA expression.
This table summarizes PNMT 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 1. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for PNMT. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PNMT shows lower tumor expression in KIRC, KIRP, LUAD, LUSC and UCEC and higher tumor expression in THCA. The KIRC box plot shows higher PNMT RNA expression in normal versus tumor tissue (log2 FC = −1.287, t-test p < 0.001).
This table shows molecular features associated with PNMT in patient tissues and cancer cell lines. In patient samples, PNMT shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, PNMT RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in KIDNEY and BLOOD_Leukemia.
