Q-omics provides the consensus-scored ASAP3 profile across patient tissues and cancer cell-line models. ASAP3 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, ASAP3 is differentially expressed in 12, with the highest sampling consensus in COAD. Additionally, ASAP3 RNA expression shows 19,366 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight HNSC, COAD, and THYM as cancer lineages where ASAP3 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 ASAP3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ASAP3 survival associations across molecular data types. ASAP3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (9) 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 ASAP3 RNA expression–survival associations across cancer types. High ASAP3 expression shows unfavorable associations in OV, STAD, UCEC and LGG, but favorable associations in HNSC and LUAD. The HNSC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .001). Together, the overview and detailed table identify HNSC as the clearest survival context for ASAP3 RNA expression.
This table summarizes ASAP3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 4. The strongest signals are observed in COAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for ASAP3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ASAP3 shows lower tumor expression in COAD, KIRC, THCA, LUAD and HNSC and higher tumor expression in LIHC. The COAD box plot shows higher ASAP3 RNA expression in normal versus tumor tissue (log2 FC = −1.891, t-test p < 0.001).
This table shows molecular features associated with ASAP3 in patient tissues and cancer cell lines. In patient samples, ASAP3 shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, ASAP3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LUNG_SCLC.
