Q-omics provides the consensus-scored NCL profile across patient tissues and cancer cell-line models. NCL expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, NCL is differentially expressed in 15, with the highest sampling consensus in STAD. Additionally, NCL protein abundance shows 28,268 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, STAD, and GBM as cancer lineages where NCL 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 NCL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NCL survival associations across molecular data types. NCL RNA expression shows survival associations in the most cancer types (28), followed by mutation status (6) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible NCL RNA expression–survival associations across cancer types. High NCL expression shows unfavorable associations in KIRP, ACC, LIHC, UVM and HNSC, but favorable associations in KIRC. The KIRP 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 KIRP as the clearest survival context for NCL RNA expression.
This table summarizes NCL tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 7. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for NCL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NCL shows higher tumor expression in STAD, COAD, HNSC, LIHC, LUSC and LUAD. The STAD box plot shows higher NCL RNA expression in tumor versus normal tissue (log2 FC = +1.521, t-test p < 0.001).
This table shows molecular features associated with NCL in patient tissues and cancer cell lines. In patient samples, NCL 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, NCL 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 SKIN and BLOOD_Lymphoma.
