Q-omics provides the consensus-scored NPM2 profile across patient tissues and cancer cell-line models. NPM2 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, NPM2 is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, NPM2 RNA expression shows 18,640 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, KIRC, and GBM as cancer lineages where NPM2 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 NPM2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NPM2 survival associations across molecular data types. NPM2 RNA expression shows survival associations in the most cancer types (25), 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 NPM2 RNA expression–survival associations across cancer types. High NPM2 expression shows unfavorable associations in SKCM, MESO and UCS, but favorable associations in KIRP, UVM and LUSC. The KIRP Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .002). Together, the overview and detailed table identify KIRP as the clearest survival context for NPM2 RNA expression.
This table summarizes NPM2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for NPM2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NPM2 shows lower tumor expression in KIRC, BRCA and KICH and higher tumor expression in COAD, LIHC and STAD. The KIRC box plot shows higher NPM2 RNA expression in normal versus tumor tissue (log2 FC = −1.330, t-test p < 0.001).
This table shows molecular features associated with NPM2 in patient tissues and cancer cell lines. In patient samples, NPM2 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, NPM2 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 LUNG_SCLC.
