Q-omics provides the consensus-scored PDE6A profile across patient tissues and cancer cell-line models. PDE6A expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in KICH. Among the 18 cancer types available for tumor–normal comparison, PDE6A is differentially expressed in 9, with the highest sampling consensus in COAD. Additionally, PDE6A protein abundance shows 14,611 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KICH, COAD, and GBM as cancer lineages where PDE6A 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 PDE6A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PDE6A survival associations across molecular data types. PDE6A RNA expression shows survival associations in the most cancer types (20), followed by mutation status (5) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PDE6A RNA expression–survival associations across cancer types. High PDE6A expression shows unfavorable associations in KICH, LGG, LIHC, KIRC, UVM and MESO. The KICH Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify KICH as the clearest survival context for PDE6A RNA expression.
This table summarizes PDE6A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 6. The strongest signals are observed in COAD for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for PDE6A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PDE6A shows lower tumor expression in COAD, HNSC, READ, LUSC and LUAD and higher tumor expression in KIRC. The COAD box plot shows higher PDE6A RNA expression in normal versus tumor tissue (log2 FC = −2.078, t-test p < 0.001).
This table shows molecular features associated with PDE6A in patient tissues and cancer cell lines. In patient samples, PDE6A 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, PDE6A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Myeloma, while CRISPR and shRNA rows add functional-dependency signals in BONE and BLOOD_Lymphoma.
