Q-omics provides the consensus-scored LDHD profile across patient tissues and cancer cell-line models. LDHD expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, LDHD is differentially expressed in 16, with the highest sampling consensus in THCA. Additionally, LDHD protein abundance shows 20,526 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, THCA, and GBM as cancer lineages where LDHD 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 LDHD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LDHD survival associations across molecular data types. LDHD 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 LDHD RNA expression–survival associations across cancer types. High LDHD expression shows favorable associations in KIRP, KIRC, LIHC, UVM, ACC and MESO. 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 LDHD RNA expression.
This table summarizes LDHD 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 6. The strongest signals are observed in THCA for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for LDHD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LDHD shows lower tumor expression in THCA, COAD, KIRC, HNSC, LUAD and KIRP. The THCA box plot shows higher LDHD RNA expression in normal versus tumor tissue (log2 FC = −3.492, t-test p < 0.001).
This table shows molecular features associated with LDHD in patient tissues and cancer cell lines. In patient samples, LDHD 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, LDHD 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 BLOOD_Myeloma and SOFT_TISSUE.
