Q-omics provides the consensus-scored DCAF6 profile across patient tissues and cancer cell-line models. DCAF6 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, DCAF6 is differentially expressed in 12, with the highest sampling consensus in COAD. Additionally, DCAF6 RNA expression shows 21,145 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight ACC, and COAD as cancer lineages where DCAF6 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 DCAF6 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DCAF6 survival associations across molecular data types. DCAF6 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (8) 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 DCAF6 RNA expression–survival associations across cancer types. High DCAF6 expression shows unfavorable associations in ACC, LGG and KIRP, but favorable associations in KIRC, MESO and HNSC. 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 DCAF6 RNA expression.
This table summarizes DCAF6 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 3. The strongest signals are observed in COAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for DCAF6. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DCAF6 shows lower tumor expression in COAD and higher tumor expression in KIRC, KIRP, LIHC, BRCA and CHOL. The COAD box plot shows higher DCAF6 RNA expression in normal versus tumor tissue (log2 FC = −0.379, t-test p < 0.001).
This table shows molecular features associated with DCAF6 in patient tissues and cancer cell lines. In patient samples, DCAF6 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, DCAF6 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BLOOD_Lymphoma.
