Q-omics provides the consensus-scored PTN profile across patient tissues and cancer cell-line models. PTN expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in LGG. Among the 18 cancer types available for tumor–normal comparison, PTN is differentially expressed in 14, with the highest sampling consensus in COAD. Additionally, PTN protein abundance shows 30,366 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight LGG, COAD, and PDAC as cancer lineages where PTN 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 PTN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PTN survival associations across molecular data types. PTN RNA expression shows survival associations in the most cancer types (21), followed by mutation status (6) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PTN RNA expression–survival associations across cancer types. High PTN expression shows unfavorable associations in LGG, UVM, BLCA and ACC, but favorable associations in KIRP and KIRC. The LGG 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 LGG as the clearest survival context for PTN RNA expression.
This table summarizes PTN 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 10. The strongest signals are observed in COAD for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for PTN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PTN shows lower tumor expression in COAD, HNSC, LUAD, THCA, KIRP and STAD. The COAD box plot shows higher PTN RNA expression in normal versus tumor tissue (log2 FC = −2.342, t-test p < 0.001).
This table shows molecular features associated with PTN in patient tissues and cancer cell lines. In patient samples, PTN shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, PTN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and CNS.
