ARF like GTPase 3Genealiases: ARFL3 · JBTS35 · RP83
Q-omics provides the consensus-scored ARL3 profile across patient tissues and cancer cell-line models. ARL3 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, ARL3 is differentially expressed in 13, with the highest sampling consensus in LIHC. Additionally, ARL3 protein abundance shows 26,694 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight ACC, LIHC, and PDAC as cancer lineages where ARL3 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 ARL3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ARL3 survival associations across molecular data types. ARL3 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (1) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ARL3 RNA expression–survival associations across cancer types. High ARL3 expression shows unfavorable associations in ACC and MESO, but favorable associations in KIRC, LGG, BRCA and THCA. 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 ARL3 RNA expression.
This table summarizes ARL3 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 5. The strongest signals are observed in THCA for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for ARL3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ARL3 shows lower tumor expression in THCA, KICH and KIRC and higher tumor expression in LIHC, COAD and HNSC. The LIHC box plot shows higher ARL3 RNA expression in tumor versus normal tissue (log2 FC = +0.909, t-test p < 0.001).
This table shows molecular features associated with ARL3 in patient tissues and cancer cell lines. In patient samples, ARL3 shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, ARL3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BLOOD_Leukemia.
