Q-omics provides the consensus-scored ARL5B profile across patient tissues and cancer cell-line models. ARL5B expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, ARL5B is differentially expressed in 12, with the highest sampling consensus in STAD. Additionally, ARL5B RNA expression shows 20,489 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight ACC, and STAD as cancer lineages where ARL5B 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 ARL5B — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ARL5B survival associations across molecular data types. ARL5B RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) 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 ARL5B RNA expression–survival associations across cancer types. High ARL5B expression shows unfavorable associations in ACC, LIHC and SARC, but favorable associations in KIRC, LUSC and LGG. 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 ARL5B RNA expression.
This table summarizes ARL5B 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 4. The strongest signals are observed in KIRP for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for ARL5B. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ARL5B shows lower tumor expression in KICH and higher tumor expression in STAD, KIRP, COAD, HNSC and UCEC. The STAD box plot shows higher ARL5B RNA expression in tumor versus normal tissue (log2 FC = +1.033, t-test p < 0.001).
This table shows molecular features associated with ARL5B in patient tissues and cancer cell lines. In patient samples, ARL5B 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, ARL5B RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and BLOOD_Leukemia.
