Q-omics provides the consensus-scored ARNTL profile across patient tissues and cancer cell-line models. ARNTL expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, ARNTL is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, ARNTL RNA expression shows 19,423 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight SKCM, KIRC, and UVM as cancer lineages where ARNTL 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 ARNTL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ARNTL survival associations across molecular data types. ARNTL RNA expression shows survival associations in the most cancer types (25), followed by mutation status (7) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ARNTL RNA expression–survival associations across cancer types. High ARNTL expression shows unfavorable associations in KICH, ACC and LGG, but favorable associations in SKCM, BRCA and LUAD. 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 ARNTL RNA expression.
This table summarizes ARNTL tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for ARNTL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ARNTL shows lower tumor expression in KICH, LUAD and COAD and higher tumor expression in KIRC, THCA and HNSC. The KIRC box plot shows higher ARNTL RNA expression in tumor versus normal tissue (log2 FC = +0.434, t-test p < 0.001).
This table shows molecular features associated with ARNTL in patient tissues and cancer cell lines. In patient samples, ARNTL 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, ARNTL RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUSC and BLOOD_Lymphoma.
