Q-omics provides the consensus-scored PDHB profile across patient tissues and cancer cell-line models. PDHB expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, PDHB is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, PDHB protein abundance shows 29,304 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight ACC, KIRC, and GBM as cancer lineages where PDHB 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 PDHB — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PDHB survival associations across molecular data types. PDHB RNA expression shows survival associations in the most cancer types (22), followed by mutation status (1) 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 PDHB RNA expression–survival associations across cancer types. High PDHB expression shows unfavorable associations in ACC and KICH, but favorable associations in BRCA, COAD, KIRC and KIRP. 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 PDHB RNA expression.
This table summarizes PDHB tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PDHB. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PDHB shows lower tumor expression in KIRC, HNSC, THCA, KIRP and LUSC and higher tumor expression in LIHC. The KIRC box plot shows higher PDHB RNA expression in normal versus tumor tissue (log2 FC = −1.123, t-test p < 0.001).
This table shows molecular features associated with PDHB in patient tissues and cancer cell lines. In patient samples, PDHB 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, PDHB RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in SKIN and UPPER_AERODIGESTIVE_TRACT.
