Q-omics provides the consensus-scored PDE1C profile across patient tissues and cancer cell-line models. PDE1C expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, PDE1C is differentially expressed in 17, with the highest sampling consensus in LUAD. Additionally, PDE1C RNA expression shows 16,790 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight KIRP, LUAD, and THYM as cancer lineages where PDE1C 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 PDE1C — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PDE1C survival associations across molecular data types. PDE1C RNA expression shows survival associations in the most cancer types (25), followed by mutation status (8) 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 PDE1C RNA expression–survival associations across cancer types. High PDE1C expression shows unfavorable associations in KIRP, BLCA, UCEC and CESC, but favorable associations in KIRC and PAAD. 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 PDE1C RNA expression.
This table summarizes PDE1C tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 17, while mass-spec protein shows differences in 2. The strongest signals are observed in LUAD for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for PDE1C. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PDE1C shows lower tumor expression in LUAD, COAD, BLCA, LUSC and UCEC and higher tumor expression in THCA. The LUAD box plot shows higher PDE1C RNA expression in normal versus tumor tissue (log2 FC = −1.551, t-test p < 0.001).
This table shows molecular features associated with PDE1C in patient tissues and cancer cell lines. In patient samples, PDE1C 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, PDE1C 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 KIDNEY and SKIN.
