Q-omics provides the consensus-scored NPR1 profile across patient tissues and cancer cell-line models. NPR1 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, NPR1 is differentially expressed in 15, with the highest sampling consensus in KICH. Additionally, NPR1 RNA expression shows 16,459 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRP, KICH, and LSCC as cancer lineages where NPR1 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 NPR1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NPR1 survival associations across molecular data types. NPR1 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (11) 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 NPR1 RNA expression–survival associations across cancer types. High NPR1 expression shows unfavorable associations in UVM, but favorable associations in KIRP, HNSC, MESO, PAAD and KIRC. 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 NPR1 RNA expression.
This table summarizes NPR1 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 3. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for NPR1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NPR1 shows lower tumor expression in KICH, BLCA, LUAD, THCA, KIRC and LUSC. The KICH box plot shows higher NPR1 RNA expression in normal versus tumor tissue (log2 FC = −3.700, t-test p < 0.001).
This table shows molecular features associated with NPR1 in patient tissues and cancer cell lines. In patient samples, NPR1 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, NPR1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in CNS and LARGE_INTESTINE.
