Q-omics provides the consensus-scored CEBPD profile across patient tissues and cancer cell-line models. CEBPD expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, CEBPD is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, CEBPD RNA expression shows 16,353 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight UVM, and KIRC as cancer lineages where CEBPD 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 CEBPD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CEBPD survival associations across molecular data types. CEBPD RNA expression shows survival associations in the most cancer types (21), followed by mutation status (1) 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 CEBPD RNA expression–survival associations across cancer types. High CEBPD expression shows unfavorable associations in UVM, KIRP, OV, LGG and ACC, but favorable associations in MESO. The UVM 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 UVM as the clearest survival context for CEBPD RNA expression.
This table summarizes CEBPD 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 3. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CEBPD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CEBPD shows lower tumor expression in KICH, BLCA, BRCA, LUAD and UCEC and higher tumor expression in KIRC. The KIRC box plot shows higher CEBPD RNA expression in tumor versus normal tissue (log2 FC = +0.634, t-test p < 0.001).
This table shows molecular features associated with CEBPD in patient tissues and cancer cell lines. In patient samples, CEBPD shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, CEBPD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in CNS and BONE.
