Q-omics provides the consensus-scored DEAF1 profile across patient tissues and cancer cell-line models. DEAF1 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, DEAF1 is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, DEAF1 RNA expression shows 18,642 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight ACC, and KIRC as cancer lineages where DEAF1 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 DEAF1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DEAF1 survival associations across molecular data types. DEAF1 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (7) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible DEAF1 RNA expression–survival associations across cancer types. High DEAF1 expression shows unfavorable associations in ACC, LIHC, KICH and COAD, but favorable associations in LGG and BRCA. 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 DEAF1 RNA expression.
This table summarizes DEAF1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 2. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for DEAF1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DEAF1 shows lower tumor expression in THCA and higher tumor expression in KIRC, COAD, LIHC, KIRP and CHOL. The KIRC box plot shows higher DEAF1 RNA expression in tumor versus normal tissue (log2 FC = +1.020, t-test p < 0.001).
This table shows molecular features associated with DEAF1 in patient tissues and cancer cell lines. In patient samples, DEAF1 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, DEAF1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and UPPER_AERODIGESTIVE_TRACT.
