Q-omics provides the consensus-scored NCAN profile across patient tissues and cancer cell-line models. NCAN expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, NCAN is differentially expressed in 7, with the highest sampling consensus in COAD. Additionally, NCAN RNA expression shows 12,500 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight ACC, COAD, and TGCT as cancer lineages where NCAN 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 NCAN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NCAN survival associations across molecular data types. NCAN RNA expression shows survival associations in the most cancer types (26), followed by mutation status (10) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible NCAN RNA expression–survival associations across cancer types. High NCAN expression shows unfavorable associations in ACC, KIRC, DLBC and UCS, but favorable associations in UVM and CESC. 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 NCAN RNA expression.
This table summarizes NCAN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 7. The strongest signals are observed in LUAD for RNA.
This table ranks reproducible tumor–normal expression differences for NCAN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NCAN shows lower tumor expression in COAD and THCA and higher tumor expression in LUAD, KIRP, LUSC and LIHC. The COAD box plot shows higher NCAN RNA expression in normal versus tumor tissue (log2 FC = −0.093, t-test p < 0.001).
This table shows molecular features associated with NCAN in patient tissues and cancer cell lines. In patient samples, NCAN shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, NCAN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in BONE and LARGE_INTESTINE.
