Q-omics provides the consensus-scored ADPRS profile across patient tissues and cancer cell-line models. ADPRS expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in LIHC. Among the 18 cancer types available for tumor–normal comparison, ADPRS is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, ADPRS protein abundance shows 25,272 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight LIHC, KIRC, and PDAC as cancer lineages where ADPRS 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 ADPRS — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ADPRS survival associations across molecular data types. ADPRS RNA expression shows survival associations in the most cancer types (24), followed by mutation status (2) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ADPRS RNA expression–survival associations across cancer types. High ADPRS expression shows unfavorable associations in LIHC, KICH, ACC, LGG and UCEC, but favorable associations in CHOL. The LIHC 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 LIHC as the clearest survival context for ADPRS RNA expression.
This table summarizes ADPRS 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 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for ADPRS. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ADPRS shows lower tumor expression in KICH and higher tumor expression in KIRC, BLCA, LIHC, STAD and COAD. The KIRC box plot shows higher ADPRS RNA expression in tumor versus normal tissue (log2 FC = +1.124, t-test p < 0.001).
This table shows molecular features associated with ADPRS in patient tissues and cancer cell lines. In patient samples, ADPRS shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, ADPRS RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Myeloma and LARGE_INTESTINE.
