Q-omics provides the consensus-scored NFRKB profile across patient tissues and cancer cell-line models. NFRKB expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, NFRKB is differentially expressed in 12, with the highest sampling consensus in THCA. Additionally, NFRKB RNA expression shows 20,381 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight ACC, and THCA as cancer lineages where NFRKB 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 NFRKB — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NFRKB survival associations across molecular data types. NFRKB RNA expression shows survival associations in the most cancer types (22), followed by mutation status (7) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible NFRKB RNA expression–survival associations across cancer types. High NFRKB expression shows unfavorable associations in ACC, LIHC, COAD and MESO, but favorable associations in READ and KIRC. The ACC 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 ACC as the clearest survival context for NFRKB RNA expression.
This table summarizes NFRKB tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 5. The strongest signals are observed in THCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for NFRKB. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NFRKB shows lower tumor expression in THCA, KICH and BRCA and higher tumor expression in LIHC, STAD and CHOL. The THCA box plot shows higher NFRKB RNA expression in normal versus tumor tissue (log2 FC = −0.704, t-test p < 0.001).
This table shows molecular features associated with NFRKB in patient tissues and cancer cell lines. In patient samples, NFRKB 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, NFRKB RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUSC and LARGE_INTESTINE.
