Q-omics provides the consensus-scored ACE profile across patient tissues and cancer cell-line models. ACE expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, ACE is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, ACE protein abundance shows 17,888 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, and LSCC as cancer lineages where ACE 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 ACE — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ACE survival associations across molecular data types. ACE RNA expression shows survival associations in the most cancer types (24), followed by mutation status (7) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ACE RNA expression–survival associations across cancer types. High ACE expression shows unfavorable associations in UVM, but favorable associations in KIRC, HNSC, CESC, OV and SKCM. 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 ACE RNA expression.
This table summarizes ACE tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, 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 ACE. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ACE shows lower tumor expression in LUAD, THCA and LUSC and higher tumor expression in KIRC, HNSC and LIHC. The KIRC box plot shows higher ACE RNA expression in tumor versus normal tissue (log2 FC = +1.909, t-test p < 0.001).
This table shows molecular features associated with ACE in patient tissues and cancer cell lines. In patient samples, ACE 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, ACE RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in SKIN and LARGE_INTESTINE.
