Q-omics provides the consensus-scored PPARGC1A profile across patient tissues and cancer cell-line models. PPARGC1A expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, PPARGC1A is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, PPARGC1A RNA expression shows 17,252 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight MESO, KIRC, and TGCT as cancer lineages where PPARGC1A 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 PPARGC1A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PPARGC1A survival associations across molecular data types. PPARGC1A RNA expression shows survival associations in the most cancer types (28), followed by mutation status (11). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PPARGC1A RNA expression–survival associations across cancer types. High PPARGC1A expression shows unfavorable associations in UCEC and BLCA, but favorable associations in MESO, KIRC, ACC and LIHC. The MESO 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 MESO as the clearest survival context for PPARGC1A RNA expression.
This table summarizes PPARGC1A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PPARGC1A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PPARGC1A shows lower tumor expression in KIRC, COAD, THCA, BLCA, HNSC and LUAD. The KIRC box plot shows higher PPARGC1A RNA expression in normal versus tumor tissue (log2 FC = −2.166, t-test p < 0.001).
This table shows molecular features associated with PPARGC1A in patient tissues and cancer cell lines. In patient samples, PPARGC1A shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, PPARGC1A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in STOMACH and SKIN.
