Q-omics provides the consensus-scored OAS3 profile across patient tissues and cancer cell-line models. OAS3 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, OAS3 is differentially expressed in 16, with the highest sampling consensus in HNSC. Additionally, OAS3 RNA expression shows 18,092 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight ACC, HNSC, and KIRP as cancer lineages where OAS3 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 OAS3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes OAS3 survival associations across molecular data types. OAS3 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (4) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible OAS3 RNA expression–survival associations across cancer types. High OAS3 expression shows unfavorable associations in ACC, LGG, PAAD, UCEC and HNSC, but favorable associations in KIRC. The ACC 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 ACC as the clearest survival context for OAS3 RNA expression.
This table summarizes OAS3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for OAS3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. OAS3 shows higher tumor expression in HNSC, KIRC, BLCA, STAD, BRCA and COAD. The HNSC box plot shows higher OAS3 RNA expression in tumor versus normal tissue (log2 FC = +1.985, t-test p < 0.001).
This table shows molecular features associated with OAS3 in patient tissues and cancer cell lines. In patient samples, OAS3 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, OAS3 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 OVARY and CNS.
