Q-omics provides the consensus-scored AVIL profile across patient tissues and cancer cell-line models. AVIL expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, AVIL is differentially expressed in 7, with the highest sampling consensus in COAD. Additionally, AVIL RNA expression shows 19,562 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight HNSC, COAD, and UVM as cancer lineages where AVIL 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 AVIL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes AVIL survival associations across molecular data types. AVIL RNA expression shows survival associations in the most cancer types (24), followed by mutation status (9) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible AVIL RNA expression–survival associations across cancer types. High AVIL expression shows unfavorable associations in KIRC and LGG, but favorable associations in HNSC, BLCA, SKCM and UCS. The HNSC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .006). Together, the overview and detailed table identify HNSC as the clearest survival context for AVIL RNA expression.
This table summarizes AVIL tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 7, while mass-spec protein shows differences in 5. The strongest signals are observed in COAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for AVIL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. AVIL shows lower tumor expression in COAD, THCA and KICH and higher tumor expression in LIHC, CHOL and STAD. The COAD box plot shows higher AVIL RNA expression in normal versus tumor tissue (log2 FC = −1.026, t-test p < 0.001).
This table shows molecular features associated with AVIL in patient tissues and cancer cell lines. In patient samples, AVIL 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, AVIL RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BLOOD_Leukemia.
