Q-omics provides the consensus-scored ARNT2 profile across patient tissues and cancer cell-line models. ARNT2 expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in PAAD. Among the 18 cancer types available for tumor–normal comparison, ARNT2 is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, ARNT2 RNA expression shows 18,758 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight PAAD, KIRC, and UVM as cancer lineages where ARNT2 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 ARNT2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ARNT2 survival associations across molecular data types. ARNT2 RNA expression shows survival associations in the most cancer types (20), followed by mutation status (7) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ARNT2 RNA expression–survival associations across cancer types. High ARNT2 expression shows unfavorable associations in ESCA, but favorable associations in PAAD, HNSC, UCEC, CHOL and BRCA. The PAAD 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 PAAD as the clearest survival context for ARNT2 RNA expression.
This table summarizes ARNT2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 2. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for ARNT2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ARNT2 shows lower tumor expression in KIRC, BLCA, LUAD, KIRP and LUSC and higher tumor expression in BRCA. The KIRC box plot shows higher ARNT2 RNA expression in normal versus tumor tissue (log2 FC = −1.927, t-test p < 0.001).
This table shows molecular features associated with ARNT2 in patient tissues and cancer cell lines. In patient samples, ARNT2 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, ARNT2 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 LARGE_INTESTINE and CNS.
