Q-omics provides the consensus-scored CSAD profile across patient tissues and cancer cell-line models. CSAD expression is associated with patient survival in 29 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CSAD is differentially expressed in 8, with the highest sampling consensus in KIRC. Additionally, CSAD RNA expression shows 19,477 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, and UVM as cancer lineages where CSAD 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 CSAD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CSAD survival associations across molecular data types. CSAD RNA expression shows survival associations in the most cancer types (29), followed by mutation status (2) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CSAD RNA expression–survival associations across cancer types. High CSAD expression shows unfavorable associations in KIRC and KICH, but favorable associations in BLCA, HNSC, LIHC and PAAD. The KIRC 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 KIRC as the clearest survival context for CSAD RNA expression.
This table summarizes CSAD tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for CSAD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CSAD shows lower tumor expression in LIHC, BRCA and CHOL and higher tumor expression in KIRC, COAD and READ. The KIRC box plot shows higher CSAD RNA expression in tumor versus normal tissue (log2 FC = +0.439, t-test p < 0.001).
This table shows molecular features associated with CSAD in patient tissues and cancer cell lines. In patient samples, CSAD shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, CSAD 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 SOFT_TISSUE and BREAST.
