Q-omics provides the consensus-scored AHRR profile across patient tissues and cancer cell-line models. AHRR expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, AHRR is differentially expressed in 9, with the highest sampling consensus in COAD. Additionally, AHRR RNA expression shows 17,252 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight HNSC, COAD, and UVM as cancer lineages where AHRR 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 AHRR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes AHRR survival associations across molecular data types. AHRR RNA expression shows survival associations in the most cancer types (25), followed by mutation status (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible AHRR RNA expression–survival associations across cancer types. High AHRR expression shows unfavorable associations in UVM, KIRP, KICH, BRCA and LGG, but favorable associations in HNSC. The HNSC 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 HNSC as the clearest survival context for AHRR RNA expression.
This table summarizes AHRR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 2. The strongest signals are observed in COAD for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for AHRR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. AHRR shows lower tumor expression in COAD and higher tumor expression in HNSC, KIRC, BRCA, LIHC and CHOL. The COAD box plot shows higher AHRR RNA expression in normal versus tumor tissue (log2 FC = −0.645, t-test p < 0.001).
This table shows molecular features associated with AHRR in patient tissues and cancer cell lines. In patient samples, AHRR 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, AHRR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and CNS.
