ARF like GTPase 13AGenealiases: ARL13 · dJ341D10.2
Q-omics provides the consensus-scored ARL13A profile across patient tissues and cancer cell-line models. ARL13A 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, ARL13A is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, ARL13A RNA expression shows 19,994 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight KIRC, HNSC, and KIRP as cancer lineages where ARL13A 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 ARL13A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ARL13A survival associations across molecular data types. ARL13A RNA expression shows survival associations in the most cancer types (23), followed by mutation status (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ARL13A RNA expression–survival associations across cancer types. High ARL13A expression shows unfavorable associations in KIRC, THCA, UVM and KIRP, but favorable associations in SKCM and HNSC. The KIRC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify KIRC as the clearest survival context for ARL13A RNA expression.
This table summarizes ARL13A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 1. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for ARL13A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ARL13A shows lower tumor expression in THCA and UCEC and higher tumor expression in HNSC, STAD, LUSC and KIRC. The HNSC box plot shows higher ARL13A RNA expression in tumor versus normal tissue (log2 FC = +0.322, t-test p < 0.001).
This table shows molecular features associated with ARL13A in patient tissues and cancer cell lines. In patient samples, ARL13A shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, ARL13A 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 LUNG_NSCLC_LUSC and LARGE_INTESTINE.
