Q-omics provides the consensus-scored AASS profile across patient tissues and cancer cell-line models. AASS expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in STAD. Among the 18 cancer types available for tumor–normal comparison, AASS is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, AASS RNA expression shows 20,064 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight STAD, KIRC, and THYM as cancer lineages where AASS 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 AASS — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes AASS survival associations across molecular data types. AASS RNA expression shows survival associations in the most cancer types (22), followed by mutation status (8) 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 AASS RNA expression–survival associations across cancer types. High AASS expression shows unfavorable associations in STAD, UVM and LGG, but favorable associations in BRCA, LIHC and SCLC. The STAD Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .003). Together, the overview and detailed table identify STAD as the clearest survival context for AASS RNA expression.
This table summarizes AASS tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, 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 AASS. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. AASS shows lower tumor expression in KIRC, KICH, UCEC, THCA, BRCA and KIRP. The KIRC box plot shows higher AASS RNA expression in normal versus tumor tissue (log2 FC = −1.040, t-test p < 0.001).
This table shows molecular features associated with AASS in patient tissues and cancer cell lines. In patient samples, AASS 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, AASS RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in BREAST and UPPER_AERODIGESTIVE_TRACT.
