Q-omics provides the consensus-scored ARL2-SNX15 profile across patient tissues and cancer cell-line models. ARL2-SNX15 expression is associated with patient survival in 18 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, ARL2-SNX15 is differentially expressed in 4, with the highest sampling consensus in HNSC. Additionally, ARL2-SNX15 RNA expression shows 6,476 significant gene co-expression associations, with the highest sampling consensus in ESCA. Together, these results highlight KIRC, HNSC, and ESCA as cancer lineages where ARL2-SNX15 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 ARL2-SNX15 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ARL2-SNX15 survival associations across molecular data types. ARL2-SNX15 RNA expression shows survival associations in the most cancer types (18). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ARL2-SNX15 RNA expression–survival associations across cancer types. High ARL2-SNX15 expression shows unfavorable associations in KIRC, LUSC, BRCA, UCEC and CESC, but favorable associations in COAD. The KIRC 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 KIRC as the clearest survival context for ARL2-SNX15 RNA expression.
This table summarizes ARL2-SNX15 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 4. The strongest signals are observed in HNSC for RNA.
This table ranks reproducible tumor–normal expression differences for ARL2-SNX15. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ARL2-SNX15 shows lower tumor expression in BRCA and higher tumor expression in HNSC, LUAD and LUSC. The HNSC box plot shows higher ARL2-SNX15 RNA expression in tumor versus normal tissue (log2 FC = +0.036, t-test p < 0.001).
This table shows molecular features associated with ARL2-SNX15 in patient tissues and cancer cell lines. In patient samples, ARL2-SNX15 shows the broadest associations at the RNA and protein expression levels, with ESCA recurring as the lineage with the largest associated feature set. In cancer cell lines, ARL2-SNX15 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in STOMACH.
