Q-omics provides the consensus-scored NPTN profile across patient tissues and cancer cell-line models. NPTN expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, NPTN is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, NPTN protein abundance shows 28,149 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, HNSC, and GBM as cancer lineages where NPTN 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 NPTN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NPTN survival associations across molecular data types. NPTN RNA expression shows survival associations in the most cancer types (26), followed by mutation status (5) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible NPTN RNA expression–survival associations across cancer types. High NPTN expression shows unfavorable associations in UVM, SCLC, LUAD and HNSC, but favorable associations in KIRC and SARC. The KIRC 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 KIRC as the clearest survival context for NPTN RNA expression.
This table summarizes NPTN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 5. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for NPTN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NPTN shows lower tumor expression in KIRP, THCA, UCEC and COAD and higher tumor expression in HNSC and LIHC. The HNSC box plot shows higher NPTN RNA expression in tumor versus normal tissue (log2 FC = +0.850, t-test p < 0.001).
This table shows molecular features associated with NPTN in patient tissues and cancer cell lines. In patient samples, NPTN 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, NPTN 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 PANCREAS and BONE.
