Q-omics provides the consensus-scored ARSA profile across patient tissues and cancer cell-line models. ARSA expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, ARSA is differentially expressed in 8, with the highest sampling consensus in KIRC. Additionally, ARSA protein abundance shows 21,235 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight ACC, KIRC, and GBM as cancer lineages where ARSA 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 ARSA — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ARSA survival associations across molecular data types. ARSA RNA expression shows survival associations in the most cancer types (23), followed by mutation status (3) and mass-spec protein abundance (11). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ARSA RNA expression–survival associations across cancer types. High ARSA expression shows unfavorable associations in ACC, LGG and LIHC, but favorable associations in UCEC, LUAD and PAAD. The ACC 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 ACC as the clearest survival context for ARSA RNA expression.
This table summarizes ARSA 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 4. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for ARSA. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ARSA shows lower tumor expression in COAD and READ and higher tumor expression in KIRC, LIHC, HNSC and CHOL. The KIRC box plot shows higher ARSA RNA expression in tumor versus normal tissue (log2 FC = +0.782, t-test p < 0.001).
This table shows molecular features associated with ARSA in patient tissues and cancer cell lines. In patient samples, ARSA shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, ARSA RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in OESOPHAGUS and UPPER_AERODIGESTIVE_TRACT.
