Q-omics provides the consensus-scored BDH1 profile across patient tissues and cancer cell-line models. BDH1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in LIHC. Among the 18 cancer types available for tumor–normal comparison, BDH1 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, BDH1 protein abundance shows 22,430 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight LIHC, KIRC, and GBM as cancer lineages where BDH1 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 BDH1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BDH1 survival associations across molecular data types. BDH1 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (2) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible BDH1 RNA expression–survival associations across cancer types. High BDH1 expression shows unfavorable associations in LGG and LUAD, but favorable associations in LIHC, KIRP, LUSC and CESC. The LIHC 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 LIHC as the clearest survival context for BDH1 RNA expression.
This table summarizes BDH1 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 5. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for BDH1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BDH1 shows lower tumor expression in KIRC, THCA, COAD and READ and higher tumor expression in LUAD and LUSC. The KIRC box plot shows higher BDH1 RNA expression in normal versus tumor tissue (log2 FC = −2.215, t-test p < 0.001).
This table shows molecular features associated with BDH1 in patient tissues and cancer cell lines. In patient samples, BDH1 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, BDH1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BLOOD_Lymphoma.
