Q-omics provides the consensus-scored ARSL profile across patient tissues and cancer cell-line models. ARSL expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, ARSL is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, ARSL RNA expression shows 14,554 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KIRC, and TGCT as cancer lineages where ARSL 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 ARSL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ARSL survival associations across molecular data types. ARSL RNA expression shows survival associations in the most cancer types (25), followed by mutation status (8) 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 ARSL RNA expression–survival associations across cancer types. High ARSL expression shows unfavorable associations in LGG, LUSC, STAD and LIHC, but favorable associations in KIRC and UVM. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .001). Together, the overview and detailed table identify KIRC as the clearest survival context for ARSL RNA expression.
This table summarizes ARSL tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, 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 ARSL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ARSL shows higher tumor expression in KIRC, HNSC, STAD, LUAD, THCA and BRCA. The KIRC box plot shows higher ARSL RNA expression in tumor versus normal tissue (log2 FC = +1.600, t-test p < 0.001).
This table shows molecular features associated with ARSL in patient tissues and cancer cell lines. In patient samples, ARSL shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, ARSL RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in BONE and LARGE_INTESTINE.
