Q-omics provides the consensus-scored ARL11 profile across patient tissues and cancer cell-line models. ARL11 expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, ARL11 is differentially expressed in 8, with the highest sampling consensus in KIRC. Additionally, ARL11 RNA expression shows 17,537 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight SKCM, KIRC, and UVM as cancer lineages where ARL11 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 ARL11 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ARL11 survival associations across molecular data types. ARL11 RNA expression shows survival associations in the most cancer types (19), followed by mutation status (7) 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 ARL11 RNA expression–survival associations across cancer types. High ARL11 expression shows unfavorable associations in UVM, LGG, BLCA and LIHC, but favorable associations in SKCM and KIRC. The SKCM 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 SKCM as the clearest survival context for ARL11 RNA expression.
This table summarizes ARL11 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 2. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for ARL11. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ARL11 shows lower tumor expression in LUAD and LUSC and higher tumor expression in KIRC, HNSC, KIRP and BRCA. The KIRC box plot shows higher ARL11 RNA expression in tumor versus normal tissue (log2 FC = +1.264, t-test p < 0.001).
This table shows molecular features associated with ARL11 in patient tissues and cancer cell lines. In patient samples, ARL11 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, ARL11 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and BLOOD_Lymphoma.
