Q-omics provides the consensus-scored DTD1 profile across patient tissues and cancer cell-line models. DTD1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, DTD1 is differentially expressed in 15, with the highest sampling consensus in COAD. Additionally, DTD1 RNA expression shows 19,077 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight MESO, COAD, and ACC as cancer lineages where DTD1 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 DTD1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DTD1 survival associations across molecular data types. DTD1 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (6) 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 DTD1 RNA expression–survival associations across cancer types. High DTD1 expression shows unfavorable associations in MESO, UCS, KICH and LIHC, but favorable associations in READ and LGG. The MESO 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 MESO as the clearest survival context for DTD1 RNA expression.
This table summarizes DTD1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for DTD1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DTD1 shows higher tumor expression in COAD, HNSC, KIRC, BLCA, KIRP and LIHC. The COAD box plot shows higher DTD1 RNA expression in tumor versus normal tissue (log2 FC = +1.386, t-test p < 0.001).
This table shows molecular features associated with DTD1 in patient tissues and cancer cell lines. In patient samples, DTD1 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, DTD1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in KIDNEY and BLOOD_Leukemia.
