Q-omics provides the consensus-scored DHRS2 profile across patient tissues and cancer cell-line models. DHRS2 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, DHRS2 is differentially expressed in 11, with the highest sampling consensus in COAD. Additionally, DHRS2 RNA expression shows 12,517 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight HNSC, COAD, and TGCT as cancer lineages where DHRS2 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 DHRS2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DHRS2 survival associations across molecular data types. DHRS2 RNA expression shows survival associations in the most cancer types (24), 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 DHRS2 RNA expression–survival associations across cancer types. High DHRS2 expression shows unfavorable associations in HNSC, KIRC, UVM, ACC and UCS, but favorable associations in STAD. The HNSC 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 HNSC as the clearest survival context for DHRS2 RNA expression.
This table summarizes DHRS2 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 3. The strongest signals are observed in COAD for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for DHRS2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DHRS2 shows lower tumor expression in KIRC and higher tumor expression in COAD, KICH, THCA, HNSC and LUSC. The COAD box plot shows higher DHRS2 RNA expression in tumor versus normal tissue (log2 FC = +1.011, t-test p < 0.001).
This table shows molecular features associated with DHRS2 in patient tissues and cancer cell lines. In patient samples, DHRS2 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, DHRS2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in OESOPHAGUS and URINARY_TRACT.
