Q-omics provides the consensus-scored NPPB profile across patient tissues and cancer cell-line models. NPPB expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, NPPB is differentially expressed in 9, with the highest sampling consensus in HNSC. Additionally, NPPB RNA expression shows 10,040 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight MESO, HNSC, and TGCT as cancer lineages where NPPB 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 NPPB — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NPPB survival associations across molecular data types. NPPB RNA expression shows survival associations in the most cancer types (20), followed by mutation status (4) 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 NPPB RNA expression–survival associations across cancer types. High NPPB expression shows unfavorable associations in MESO, HNSC, COAD, UCS and LIHC, but favorable associations in UVM. The MESO 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 MESO as the clearest survival context for NPPB RNA expression.
This table summarizes NPPB tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9. The strongest signals are observed in HNSC for RNA.
This table ranks reproducible tumor–normal expression differences for NPPB. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NPPB shows lower tumor expression in BRCA, UCEC and KICH and higher tumor expression in HNSC, KIRP and UCEC. The HNSC box plot shows higher NPPB RNA expression in tumor versus normal tissue (log2 FC = +0.121, t-test p = .019).
This table shows molecular features associated with NPPB in patient tissues and cancer cell lines. In patient samples, NPPB shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, NPPB RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and BLOOD_Leukemia.
