Q-omics provides the consensus-scored NCF1 profile across patient tissues and cancer cell-line models. NCF1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, NCF1 is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, NCF1 protein abundance shows 28,672 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight HNSC, KIRC, and GBM as cancer lineages where NCF1 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 NCF1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NCF1 survival associations across molecular data types. NCF1 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) 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 NCF1 RNA expression–survival associations across cancer types. High NCF1 expression shows unfavorable associations in LGG and UVM, but favorable associations in HNSC, SKCM, CESC and LUAD. 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 NCF1 RNA expression.
This table summarizes NCF1 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 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for NCF1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NCF1 shows lower tumor expression in COAD, LUAD and LUSC and higher tumor expression in KIRC, KIRP and STAD. The KIRC box plot shows higher NCF1 RNA expression in tumor versus normal tissue (log2 FC = +1.557, t-test p < 0.001).
This table shows molecular features associated with NCF1 in patient tissues and cancer cell lines. In patient samples, NCF1 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, NCF1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and BLOOD_Lymphoma.
