Q-omics provides the consensus-scored PPARD profile across patient tissues and cancer cell-line models. PPARD expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in BRCA. Among the 18 cancer types available for tumor–normal comparison, PPARD is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, PPARD RNA expression shows 20,024 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight BRCA, HNSC, and THYM as cancer lineages where PPARD 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 PPARD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PPARD survival associations across molecular data types. PPARD RNA expression shows survival associations in the most cancer types (24), followed by mutation status (7) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PPARD RNA expression–survival associations across cancer types. High PPARD expression shows unfavorable associations in BRCA, DLBC, LIHC, SARC and LGG, but favorable associations in ACC. The BRCA 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 BRCA as the clearest survival context for PPARD RNA expression.
This table summarizes PPARD 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 2. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for PPARD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PPARD shows lower tumor expression in COAD and THCA and higher tumor expression in HNSC, KIRC, LIHC and BRCA. The HNSC box plot shows higher PPARD RNA expression in tumor versus normal tissue (log2 FC = +1.328, t-test p < 0.001).
This table shows molecular features associated with PPARD in patient tissues and cancer cell lines. In patient samples, PPARD 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, PPARD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BONE.
