Q-omics provides the consensus-scored DCDC2 profile across patient tissues and cancer cell-line models. DCDC2 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, DCDC2 is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, DCDC2 RNA expression shows 17,366 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight MESO, KIRC, and KIRP as cancer lineages where DCDC2 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 DCDC2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DCDC2 survival associations across molecular data types. DCDC2 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (2) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible DCDC2 RNA expression–survival associations across cancer types. High DCDC2 expression shows unfavorable associations in MESO, LUSC, LGG, ESCA and CESC, but favorable associations in CHOL. The MESO Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify MESO as the clearest survival context for DCDC2 RNA expression.
This table summarizes DCDC2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 4. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for DCDC2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DCDC2 shows lower tumor expression in KIRC, LUSC, KICH, LUAD and BRCA and higher tumor expression in COAD. The KIRC box plot shows higher DCDC2 RNA expression in normal versus tumor tissue (log2 FC = −2.212, t-test p < 0.001).
This table shows molecular features associated with DCDC2 in patient tissues and cancer cell lines. In patient samples, DCDC2 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, DCDC2 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 LARGE_INTESTINE and BONE.
