Q-omics provides the consensus-scored CENATAC-DT profile across patient tissues and cancer cell-line models. CENATAC-DT expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CENATAC-DT is differentially expressed in 8, with the highest sampling consensus in THCA. Additionally, CENATAC-DT RNA expression shows 20,035 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, THCA, and ACC as cancer lineages where CENATAC-DT 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 CENATAC-DT — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CENATAC-DT survival associations across molecular data types. CENATAC-DT RNA expression shows survival associations in the most cancer types (23). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CENATAC-DT RNA expression–survival associations across cancer types. High CENATAC-DT expression shows unfavorable associations in LIHC and ACC, but favorable associations in KIRC, UVM, READ and BRCA. The KIRC 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 KIRC as the clearest survival context for CENATAC-DT RNA expression.
This table summarizes CENATAC-DT tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8. The strongest signals are observed in THCA for RNA.
This table ranks reproducible tumor–normal expression differences for CENATAC-DT. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CENATAC-DT shows lower tumor expression in THCA and KICH and higher tumor expression in COAD, BLCA, LIHC and STAD. The THCA box plot shows higher CENATAC-DT RNA expression in normal versus tumor tissue (log2 FC = −0.790, t-test p < 0.001).
This table shows molecular features associated with CENATAC-DT in patient tissues and cancer cell lines. In patient samples, CENATAC-DT shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set.
