Q-omics provides the consensus-scored PDE4D profile across patient tissues and cancer cell-line models. PDE4D expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PDE4D is differentially expressed in 11, with the highest sampling consensus in THCA. Additionally, PDE4D RNA expression shows 19,103 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight KIRC, THCA, and KIRP as cancer lineages where PDE4D 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 PDE4D — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PDE4D survival associations across molecular data types. PDE4D RNA expression shows survival associations in the most cancer types (24), followed by mutation status (7) 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 PDE4D RNA expression–survival associations across cancer types. High PDE4D expression shows unfavorable associations in ACC, LIHC, UVM and CESC, but favorable associations in KIRC and SARC. 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 PDE4D RNA expression.
This table summarizes PDE4D tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 4. The strongest signals are observed in THCA for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for PDE4D. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PDE4D shows lower tumor expression in THCA, COAD, BLCA, LUSC, LUAD and KICH. The THCA box plot shows higher PDE4D RNA expression in normal versus tumor tissue (log2 FC = −1.880, t-test p < 0.001).
This table shows molecular features associated with PDE4D in patient tissues and cancer cell lines. In patient samples, PDE4D shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, PDE4D RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and UPPER_AERODIGESTIVE_TRACT.
