Q-omics provides the consensus-scored MDH1 profile across patient tissues and cancer cell-line models. MDH1 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, MDH1 is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, MDH1 protein abundance shows 31,387 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight LUAD, KIRC, and GBM as cancer lineages where MDH1 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 MDH1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MDH1 survival associations across molecular data types. MDH1 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (6) 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 MDH1 RNA expression–survival associations across cancer types. High MDH1 expression shows unfavorable associations in LUAD, UVM, LIHC, KICH and ESCA, but favorable associations in LUSC. The LUAD Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify LUAD as the clearest survival context for MDH1 RNA expression.
This table summarizes MDH1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, 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 MDH1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MDH1 shows lower tumor expression in KIRC, BRCA, KICH and COAD and higher tumor expression in LIHC and LUSC. The KIRC box plot shows higher MDH1 RNA expression in normal versus tumor tissue (log2 FC = −0.702, t-test p < 0.001).
This table shows molecular features associated with MDH1 in patient tissues and cancer cell lines. In patient samples, MDH1 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, MDH1 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 CNS and UPPER_AERODIGESTIVE_TRACT.
