Q-omics provides the consensus-scored ARL8A profile across patient tissues and cancer cell-line models. ARL8A 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, ARL8A is differentially expressed in 12, with the highest sampling consensus in COAD. Additionally, ARL8A RNA expression shows 19,636 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight ACC, and COAD as cancer lineages where ARL8A 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 ARL8A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ARL8A survival associations across molecular data types. ARL8A RNA expression shows survival associations in the most cancer types (23), followed by mutation status (1) 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 ARL8A RNA expression–survival associations across cancer types. High ARL8A expression shows unfavorable associations in ACC, KIRP, HNSC, CESC and COAD, but favorable associations in KIRC. 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 ARL8A RNA expression.
This table summarizes ARL8A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 6. The strongest signals are observed in COAD for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for ARL8A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ARL8A shows lower tumor expression in KICH and higher tumor expression in COAD, HNSC, LIHC, KIRP and KIRC. The COAD box plot shows higher ARL8A RNA expression in tumor versus normal tissue (log2 FC = +1.088, t-test p < 0.001).
This table shows molecular features associated with ARL8A in patient tissues and cancer cell lines. In patient samples, ARL8A shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, ARL8A 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 OVARY and UPPER_AERODIGESTIVE_TRACT.
