Q-omics provides the consensus-scored ALDOA profile across patient tissues and cancer cell-line models. ALDOA expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, ALDOA is differentially expressed in 16, with the highest sampling consensus in KIRC. Additionally, ALDOA RNA expression shows 19,100 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight LUAD, KIRC, and THYM as cancer lineages where ALDOA 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 ALDOA — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ALDOA survival associations across molecular data types. ALDOA RNA expression shows survival associations in the most cancer types (28), followed by mutation status (3) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ALDOA RNA expression–survival associations across cancer types. High ALDOA expression shows unfavorable associations in LUAD, LIHC, HNSC, BLCA, UCS and THCA. The LUAD 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 LUAD as the clearest survival context for ALDOA RNA expression.
This table summarizes ALDOA tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 4. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for ALDOA. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ALDOA shows higher tumor expression in KIRC, KIRP, LUAD, LIHC, LUSC and BRCA. The KIRC box plot shows higher ALDOA RNA expression in tumor versus normal tissue (log2 FC = +1.785, t-test p < 0.001).
This table shows molecular features associated with ALDOA in patient tissues and cancer cell lines. In patient samples, ALDOA shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, ALDOA RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in BREAST and CNS.
