Q-omics provides the consensus-scored PDE4C profile across patient tissues and cancer cell-line models. PDE4C expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, PDE4C is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, PDE4C RNA expression shows 15,381 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight KIRP, and HNSC as cancer lineages where PDE4C 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 PDE4C — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PDE4C survival associations across molecular data types. PDE4C RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PDE4C RNA expression–survival associations across cancer types. High PDE4C expression shows unfavorable associations in KIRP, KIRC, ACC, KICH, ESCA and LUSC. 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 PDE4C RNA expression.
This table summarizes PDE4C 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 1. The strongest signals are observed in HNSC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for PDE4C. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PDE4C shows lower tumor expression in HNSC, LUAD, KIRP and LUSC and higher tumor expression in THCA and LIHC. The HNSC box plot shows higher PDE4C RNA expression in normal versus tumor tissue (log2 FC = −0.745, t-test p < 0.001).
This table shows molecular features associated with PDE4C in patient tissues and cancer cell lines. In patient samples, PDE4C 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, PDE4C RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in BONE and SOFT_TISSUE.
