Q-omics provides the consensus-scored NAMPT profile across patient tissues and cancer cell-line models. NAMPT 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, NAMPT is differentially expressed in 7, with the highest sampling consensus in KIRP. Additionally, NAMPT protein abundance shows 28,441 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, and GBM as cancer lineages where NAMPT 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 NAMPT — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NAMPT survival associations across molecular data types. NAMPT RNA expression shows survival associations in the most cancer types (25), followed by mutation status (1) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible NAMPT RNA expression–survival associations across cancer types. High NAMPT expression shows unfavorable associations in KIRP, HNSC, LGG, KICH and CESC, but favorable associations in COAD. The KIRP 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 KIRP as the clearest survival context for NAMPT RNA expression.
This table summarizes NAMPT tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 7, while mass-spec protein shows differences in 9. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for NAMPT. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NAMPT shows lower tumor expression in BRCA and LIHC and higher tumor expression in KIRP, KIRC, THCA and COAD. The KIRP box plot shows higher NAMPT RNA expression in tumor versus normal tissue (log2 FC = +0.801, t-test p < 0.001).
This table shows molecular features associated with NAMPT in patient tissues and cancer cell lines. In patient samples, NAMPT 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, NAMPT RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Myeloma, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and CNS.
