Q-omics provides the consensus-scored PDE2A profile across patient tissues and cancer cell-line models. PDE2A expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PDE2A is differentially expressed in 15, with the highest sampling consensus in BLCA. Additionally, PDE2A protein abundance shows 31,736 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, BLCA, and GBM as cancer lineages where PDE2A 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 PDE2A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PDE2A survival associations across molecular data types. PDE2A RNA expression shows survival associations in the most cancer types (28), followed by mutation status (9) 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 PDE2A RNA expression–survival associations across cancer types. High PDE2A expression shows unfavorable associations in ACC, BLCA and OV, but favorable associations in KIRC, LIHC and LGG. 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 PDE2A RNA expression.
This table summarizes PDE2A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 6. The strongest signals are observed in LUAD for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for PDE2A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PDE2A shows lower tumor expression in BLCA, KIRP, COAD, LUAD, KICH and THCA. The BLCA box plot shows higher PDE2A RNA expression in normal versus tumor tissue (log2 FC = −3.707, t-test p < 0.001).
This table shows molecular features associated with PDE2A in patient tissues and cancer cell lines. In patient samples, PDE2A 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, PDE2A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in OESOPHAGUS and LARGE_INTESTINE.
