Q-omics provides the consensus-scored NFIA profile across patient tissues and cancer cell-line models. NFIA 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, NFIA is differentially expressed in 10, with the highest sampling consensus in BLCA. Additionally, NFIA protein abundance shows 23,550 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRC, BLCA, and LUAD as cancer lineages where NFIA 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 NFIA — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NFIA survival associations across molecular data types. NFIA RNA expression shows survival associations in the most cancer types (26), followed by mutation status (7) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible NFIA RNA expression–survival associations across cancer types. High NFIA expression shows unfavorable associations in ACC, but favorable associations in KIRC, UVM, KIRP, MESO and HNSC. 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 NFIA RNA expression.
This table summarizes NFIA tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 7. The strongest signals are observed in THCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for NFIA. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NFIA shows lower tumor expression in BLCA, THCA, KICH, LUAD and HNSC and higher tumor expression in KIRC. The BLCA box plot shows higher NFIA RNA expression in normal versus tumor tissue (log2 FC = −1.533, t-test p < 0.001).
This table shows molecular features associated with NFIA in patient tissues and cancer cell lines. In patient samples, NFIA shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, NFIA RNA and mutation anchors are most strongly linked to RNA-expression features, especially in STOMACH, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LARGE_INTESTINE.
