Q-omics provides the consensus-scored DCAF5 profile across patient tissues and cancer cell-line models. DCAF5 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, DCAF5 is differentially expressed in 10, with the highest sampling consensus in THCA. Additionally, DCAF5 RNA expression shows 21,150 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight ACC, and THCA as cancer lineages where DCAF5 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 DCAF5 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DCAF5 survival associations across molecular data types. DCAF5 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (5) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible DCAF5 RNA expression–survival associations across cancer types. High DCAF5 expression shows unfavorable associations in ACC and KICH, but favorable associations in KIRC, BRCA, UCS and ESCA. The ACC 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 ACC as the clearest survival context for DCAF5 RNA expression.
This table summarizes DCAF5 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 7. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for DCAF5. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DCAF5 shows lower tumor expression in THCA, COAD, BRCA and LUSC and higher tumor expression in HNSC and LIHC. The THCA box plot shows higher DCAF5 RNA expression in normal versus tumor tissue (log2 FC = −0.340, t-test p < 0.001).
This table shows molecular features associated with DCAF5 in patient tissues and cancer cell lines. In patient samples, DCAF5 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, DCAF5 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BLOOD_Leukemia.
