Q-omics provides the consensus-scored NFKBIL1 profile across patient tissues and cancer cell-line models. NFKBIL1 expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, NFKBIL1 is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, NFKBIL1 RNA expression shows 18,620 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight MESO, KIRC, and ACC as cancer lineages where NFKBIL1 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 NFKBIL1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NFKBIL1 survival associations across molecular data types. NFKBIL1 RNA expression shows survival associations in the most cancer types (28), followed by mutation status (4) 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 NFKBIL1 RNA expression–survival associations across cancer types. High NFKBIL1 expression shows unfavorable associations in ACC, KICH and LIHC, but favorable associations in MESO, LGG and READ. The MESO Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .001). Together, the overview and detailed table identify MESO as the clearest survival context for NFKBIL1 RNA expression.
This table summarizes NFKBIL1 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 2. The strongest signals are observed in KIRC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for NFKBIL1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NFKBIL1 shows lower tumor expression in UCEC and higher tumor expression in KIRC, LIHC, HNSC, CHOL and LUSC. The KIRC box plot shows higher NFKBIL1 RNA expression in tumor versus normal tissue (log2 FC = +0.777, t-test p < 0.001).
This table shows molecular features associated with NFKBIL1 in patient tissues and cancer cell lines. In patient samples, NFKBIL1 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, NFKBIL1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BLOOD_Leukemia.
