Q-omics provides the consensus-scored ARL4D profile across patient tissues and cancer cell-line models. ARL4D expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, ARL4D is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, ARL4D RNA expression shows 15,459 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight HNSC, KIRC, and THYM as cancer lineages where ARL4D 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 ARL4D — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ARL4D survival associations across molecular data types. ARL4D RNA expression shows survival associations in the most cancer types (27), 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 ARL4D RNA expression–survival associations across cancer types. High ARL4D expression shows unfavorable associations in HNSC, KIRC, LUAD, SKCM and PAAD, but favorable associations in UCEC. The HNSC 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 HNSC as the clearest survival context for ARL4D RNA expression.
This table summarizes ARL4D tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for ARL4D. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ARL4D shows lower tumor expression in KIRC, THCA, COAD, KICH and STAD and higher tumor expression in LUSC. The KIRC box plot shows higher ARL4D RNA expression in normal versus tumor tissue (log2 FC = −3.179, t-test p < 0.001).
This table shows molecular features associated with ARL4D in patient tissues and cancer cell lines. In patient samples, ARL4D shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, ARL4D 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 UPPER_AERODIGESTIVE_TRACT and BONE.
