Q-omics provides the consensus-scored DDAH1 profile across patient tissues and cancer cell-line models. DDAH1 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, DDAH1 is differentially expressed in 12, with the highest sampling consensus in KICH. Additionally, DDAH1 protein abundance shows 34,608 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, KICH, and GBM as cancer lineages where DDAH1 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 DDAH1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DDAH1 survival associations across molecular data types. DDAH1 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (5) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible DDAH1 RNA expression–survival associations across cancer types. High DDAH1 expression shows unfavorable associations in UVM, MESO and LAML, but favorable associations in KIRC, SKCM and BRCA. 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 DDAH1 RNA expression.
This table summarizes DDAH1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 6. The strongest signals are observed in KICH for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for DDAH1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DDAH1 shows lower tumor expression in KICH, KIRP, KIRC, LUSC and BLCA and higher tumor expression in STAD. The KICH box plot shows higher DDAH1 RNA expression in normal versus tumor tissue (log2 FC = −2.964, t-test p < 0.001).
This table shows molecular features associated with DDAH1 in patient tissues and cancer cell lines. In patient samples, DDAH1 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, DDAH1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in CNS and UPPER_AERODIGESTIVE_TRACT.
