Q-omics provides the consensus-scored PDHX profile across patient tissues and cancer cell-line models. PDHX expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, PDHX is differentially expressed in 10, with the highest sampling consensus in LIHC. Additionally, PDHX protein abundance shows 23,673 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight ACC, LIHC, and GBM as cancer lineages where PDHX 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 PDHX — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PDHX survival associations across molecular data types. PDHX RNA expression shows survival associations in the most cancer types (19), followed by mutation status (4) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PDHX RNA expression–survival associations across cancer types. High PDHX expression shows unfavorable associations in ACC, ESCA, LIHC and KICH, but favorable associations in KIRC and LGG. The ACC 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 ACC as the clearest survival context for PDHX RNA expression.
This table summarizes PDHX tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 8. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PDHX. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PDHX shows lower tumor expression in THCA and KIRC and higher tumor expression in LIHC, STAD, UCEC and LUSC. The LIHC box plot shows higher PDHX RNA expression in tumor versus normal tissue (log2 FC = +0.509, t-test p < 0.001).
This table shows molecular features associated with PDHX in patient tissues and cancer cell lines. In patient samples, PDHX 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, PDHX RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BLOOD_Lymphoma.
