Q-omics provides the consensus-scored DMGDH profile across patient tissues and cancer cell-line models. DMGDH expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, DMGDH is differentially expressed in 16, with the highest sampling consensus in KICH. Additionally, DMGDH RNA expression shows 17,834 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight KIRC, KICH, and THYM as cancer lineages where DMGDH 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 DMGDH — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DMGDH survival associations across molecular data types. DMGDH RNA expression shows survival associations in the most cancer types (21), followed by mutation status (7) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible DMGDH RNA expression–survival associations across cancer types. High DMGDH expression shows unfavorable associations in OV, but favorable associations in KIRC, ACC, HNSC, LIHC and MESO. The KIRC 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 KIRC as the clearest survival context for DMGDH RNA expression.
This table summarizes DMGDH tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 1. The strongest signals are observed in KICH for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for DMGDH. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DMGDH shows lower tumor expression in KICH, BLCA, THCA, KIRP and LIHC and higher tumor expression in LUAD. The KICH box plot shows higher DMGDH RNA expression in normal versus tumor tissue (log2 FC = −4.228, t-test p < 0.001).
This table shows molecular features associated with DMGDH in patient tissues and cancer cell lines. In patient samples, DMGDH shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, DMGDH 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 BLOOD_Lymphoma and LARGE_INTESTINE.
