Q-omics provides the consensus-scored NPIPB6 profile across patient tissues and cancer cell-line models. NPIPB6 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, NPIPB6 is differentially expressed in 6, with the highest sampling consensus in KIRP. Additionally, NPIPB6 RNA expression shows 13,934 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight ACC, KIRP, and UVM as cancer lineages where NPIPB6 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 NPIPB6 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NPIPB6 survival associations across molecular data types. NPIPB6 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible NPIPB6 RNA expression–survival associations across cancer types. High NPIPB6 expression shows unfavorable associations in ACC and KIRC, but favorable associations in BLCA, LGG, UCS and SKCM. The ACC 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 ACC as the clearest survival context for NPIPB6 RNA expression.
This table summarizes NPIPB6 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 6. The strongest signals are observed in KIRP for RNA.
This table ranks reproducible tumor–normal expression differences for NPIPB6. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NPIPB6 shows lower tumor expression in THCA and COAD and higher tumor expression in KIRP, HNSC, LUSC and CHOL. The KIRP box plot shows higher NPIPB6 RNA expression in tumor versus normal tissue (log2 FC = +0.457, t-test p < 0.001).
This table shows molecular features associated with NPIPB6 in patient tissues and cancer cell lines. In patient samples, NPIPB6 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, NPIPB6 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LUNG_SCLC.
