Q-omics provides the consensus-scored BRDT profile across patient tissues and cancer cell-line models. BRDT expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in SCLC. Among the 18 cancer types available for tumor–normal comparison, BRDT is differentially expressed in 9, with the highest sampling consensus in HNSC. Additionally, BRDT RNA expression shows 8,485 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight SCLC, HNSC, and TGCT as cancer lineages where BRDT 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 BRDT — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BRDT survival associations across molecular data types. BRDT RNA expression shows survival associations in the most cancer types (22), followed by mutation status (6) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible BRDT RNA expression–survival associations across cancer types. High BRDT expression shows unfavorable associations in KIRC, ACC, KICH and LIHC, but favorable associations in SCLC and OV. The SCLC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify SCLC as the clearest survival context for BRDT RNA expression.
This table summarizes BRDT tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 6. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for BRDT. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BRDT shows lower tumor expression in KICH and higher tumor expression in HNSC, LUAD, KIRC, BRCA and COAD. The HNSC box plot shows higher BRDT RNA expression in tumor versus normal tissue (log2 FC = +0.021, t-test p = .004).
This table shows molecular features associated with BRDT in patient tissues and cancer cell lines. In patient samples, BRDT shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, BRDT 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 OVARY and LARGE_INTESTINE.
