Q-omics provides the consensus-scored NONO profile across patient tissues and cancer cell-line models. NONO expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, NONO is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, NONO protein abundance shows 30,685 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight MESO, HNSC, and LSCC as cancer lineages where NONO 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 NONO — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NONO survival associations across molecular data types. NONO RNA expression shows survival associations in the most cancer types (26), followed by mutation status (6) 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 NONO RNA expression–survival associations across cancer types. High NONO expression shows unfavorable associations in MESO, KIRP, ACC and LIHC, but favorable associations in KIRC and OV. The MESO 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 MESO as the clearest survival context for NONO RNA expression.
This table summarizes NONO 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 5. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for NONO. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NONO shows higher tumor expression in HNSC, BLCA, COAD, LIHC, STAD and LUAD. The HNSC box plot shows higher NONO RNA expression in tumor versus normal tissue (log2 FC = +0.930, t-test p < 0.001).
This table shows molecular features associated with NONO in patient tissues and cancer cell lines. In patient samples, NONO shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, NONO RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BLOOD_Leukemia.
