Q-omics provides the consensus-scored PDE1A profile across patient tissues and cancer cell-line models. PDE1A expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, PDE1A is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, PDE1A protein abundance shows 29,798 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, KIRC, and GBM as cancer lineages where PDE1A 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 PDE1A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PDE1A survival associations across molecular data types. PDE1A RNA expression shows survival associations in the most cancer types (21), 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 PDE1A RNA expression–survival associations across cancer types. High PDE1A expression shows unfavorable associations in KIRP, UVM, BLCA and ESCA, but favorable associations in LGG and THCA. The KIRP 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 KIRP as the clearest survival context for PDE1A RNA expression.
This table summarizes PDE1A 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 8. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PDE1A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PDE1A shows lower tumor expression in KIRC, BLCA, KICH, COAD, UCEC and KIRP. The KIRC box plot shows higher PDE1A RNA expression in normal versus tumor tissue (log2 FC = −3.419, t-test p < 0.001).
This table shows molecular features associated with PDE1A in patient tissues and cancer cell lines. In patient samples, PDE1A shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, PDE1A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and KIDNEY.
