Q-omics provides the consensus-scored ARSD profile across patient tissues and cancer cell-line models. ARSD 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, ARSD is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, ARSD RNA expression shows 18,801 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight KIRC, and THYM as cancer lineages where ARSD 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 ARSD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ARSD survival associations across molecular data types. ARSD RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) 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 ARSD RNA expression–survival associations across cancer types. High ARSD expression shows unfavorable associations in UVM, CESC and LGG, but favorable associations in KIRC, OV and UCEC. 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 ARSD RNA expression.
This table summarizes ARSD 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 COAD for protein.
This table ranks reproducible tumor–normal expression differences for ARSD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ARSD shows lower tumor expression in KIRC, KICH, LUSC and KIRP and higher tumor expression in LUAD and STAD. The KIRC box plot shows higher ARSD RNA expression in normal versus tumor tissue (log2 FC = −0.927, t-test p < 0.001).
This table shows molecular features associated with ARSD in patient tissues and cancer cell lines. In patient samples, ARSD 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, ARSD 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 UPPER_AERODIGESTIVE_TRACT and CNS.
