Q-omics provides the consensus-scored NFKBID profile across patient tissues and cancer cell-line models. NFKBID expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, NFKBID is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, NFKBID RNA expression shows 16,618 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight HNSC, KIRC, and UVM as cancer lineages where NFKBID 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 NFKBID — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NFKBID survival associations across molecular data types. NFKBID RNA expression shows survival associations in the most cancer types (27), followed by mutation status (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible NFKBID RNA expression–survival associations across cancer types. High NFKBID expression shows unfavorable associations in OV, KIRC, THCA and LGG, but favorable associations in HNSC and BLCA. The HNSC 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 HNSC as the clearest survival context for NFKBID RNA expression.
This table summarizes NFKBID tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for NFKBID. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NFKBID shows lower tumor expression in BRCA, LUSC and KICH and higher tumor expression in KIRC, COAD and CHOL. The KIRC box plot shows higher NFKBID RNA expression in tumor versus normal tissue (log2 FC = +1.117, t-test p < 0.001).
This table shows molecular features associated with NFKBID in patient tissues and cancer cell lines. In patient samples, NFKBID 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, NFKBID RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in SKIN and UPPER_AERODIGESTIVE_TRACT.