Q-omics provides the consensus-scored DHRSX profile across patient tissues and cancer cell-line models. DHRSX expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, DHRSX is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, DHRSX RNA expression shows 18,037 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight LUAD, KIRC, and ACC as cancer lineages where DHRSX 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 DHRSX — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DHRSX survival associations across molecular data types. DHRSX RNA expression shows survival associations in the most cancer types (23), followed by mutation status (5) 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 DHRSX RNA expression–survival associations across cancer types. High DHRSX expression shows unfavorable associations in LUAD, KIRP, LGG and STAD, but favorable associations in DLBC and UCEC. The LUAD Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify LUAD as the clearest survival context for DHRSX RNA expression.
This table summarizes DHRSX tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 3. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for DHRSX. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DHRSX shows lower tumor expression in KICH and higher tumor expression in KIRC, HNSC, LIHC, LUAD and COAD. The KIRC box plot shows higher DHRSX RNA expression in tumor versus normal tissue (log2 FC = +0.993, t-test p < 0.001).
This table shows molecular features associated with DHRSX in patient tissues and cancer cell lines. In patient samples, DHRSX shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, DHRSX RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and CNS.
