Q-omics provides the consensus-scored BDH2 profile across patient tissues and cancer cell-line models. BDH2 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, BDH2 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, BDH2 protein abundance shows 27,872 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRP, KIRC, and LSCC as cancer lineages where BDH2 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 BDH2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BDH2 survival associations across molecular data types. BDH2 RNA expression shows survival associations in the most cancer types (24), 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 BDH2 RNA expression–survival associations across cancer types. High BDH2 expression shows unfavorable associations in UVM and STAD, but favorable associations in KIRP, KIRC, MESO and ACC. The KIRP 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 KIRP as the clearest survival context for BDH2 RNA expression.
This table summarizes BDH2 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 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for BDH2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BDH2 shows lower tumor expression in KIRC, KICH, KIRP, COAD, LUAD and LIHC. The KIRC box plot shows higher BDH2 RNA expression in normal versus tumor tissue (log2 FC = −0.841, t-test p < 0.001).
This table shows molecular features associated with BDH2 in patient tissues and cancer cell lines. In patient samples, BDH2 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, BDH2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and BLOOD_Leukemia.
