Q-omics provides the consensus-scored SDHD profile across patient tissues and cancer cell-line models. SDHD expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, SDHD is differentially expressed in 13, with the highest sampling consensus in THCA. Additionally, SDHD RNA expression shows 18,826 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, THCA, and UVM as cancer lineages where SDHD 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 SDHD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SDHD survival associations across molecular data types. SDHD RNA expression shows survival associations in the most cancer types (23), followed by mutation status (5) 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 SDHD RNA expression–survival associations across cancer types. High SDHD expression shows unfavorable associations in UVM, LAML, LUAD and HNSC, but favorable associations in KIRC and LUSC. 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 SDHD RNA expression.
This table summarizes SDHD tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 6. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for SDHD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SDHD shows lower tumor expression in THCA, KIRP, KIRC, COAD, BLCA and BRCA. The THCA box plot shows higher SDHD RNA expression in normal versus tumor tissue (log2 FC = −1.320, t-test p < 0.001).
This table shows molecular features associated with SDHD in patient tissues and cancer cell lines. In patient samples, SDHD shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, SDHD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and BREAST.
