Q-omics provides the consensus-scored HPN profile across patient tissues and cancer cell-line models. HPN expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, HPN is differentially expressed in 10, with the highest sampling consensus in COAD. Additionally, HPN RNA expression shows 19,711 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, COAD, and GBM as cancer lineages where HPN 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 HPN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HPN survival associations across molecular data types. HPN RNA expression shows survival associations in the most cancer types (25), followed by mutation status (7) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible HPN RNA expression–survival associations across cancer types. High HPN expression shows unfavorable associations in BLCA, LUSC and UVM, but favorable associations in KIRP, KIRC and BRCA. The KIRP Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRP as the clearest survival context for HPN RNA expression.
This table summarizes HPN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 2. The strongest signals are observed in COAD for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for HPN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HPN shows lower tumor expression in LUSC, KICH and KIRP and higher tumor expression in COAD, THCA and BRCA. The COAD box plot shows higher HPN RNA expression in tumor versus normal tissue (log2 FC = +0.909, t-test p < 0.001).
This table shows molecular features associated with HPN in patient tissues and cancer cell lines. In patient samples, HPN 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, HPN 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 LARGE_INTESTINE and LIVER.
