Q-omics provides the consensus-scored ADPRH profile across patient tissues and cancer cell-line models. ADPRH expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, ADPRH is differentially expressed in 14, with the highest sampling consensus in KICH. Additionally, ADPRH protein abundance shows 25,611 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, KICH, and LSCC as cancer lineages where ADPRH 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 ADPRH — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ADPRH survival associations across molecular data types. ADPRH RNA expression shows survival associations in the most cancer types (25), followed by mutation status (6) 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 ADPRH RNA expression–survival associations across cancer types. High ADPRH expression shows unfavorable associations in LGG and STAD, but favorable associations in KIRC, UVM, BRCA and HNSC. The KIRC 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 KIRC as the clearest survival context for ADPRH RNA expression.
This table summarizes ADPRH tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 5. The strongest signals are observed in KICH for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for ADPRH. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ADPRH shows lower tumor expression in KICH, THCA, LUAD, LUSC and BRCA and higher tumor expression in KIRC. The KICH box plot shows higher ADPRH RNA expression in normal versus tumor tissue (log2 FC = −1.911, t-test p < 0.001).
This table shows molecular features associated with ADPRH in patient tissues and cancer cell lines. In patient samples, ADPRH shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, ADPRH RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BONE.
