Q-omics provides the consensus-scored BRD2 profile across patient tissues and cancer cell-line models. BRD2 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, BRD2 is differentially expressed in 10, with the highest sampling consensus in HNSC. Additionally, BRD2 protein abundance shows 26,008 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, HNSC, and LSCC as cancer lineages where BRD2 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 BRD2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BRD2 survival associations across molecular data types. BRD2 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (4) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible BRD2 RNA expression–survival associations across cancer types. High BRD2 expression shows unfavorable associations in COAD, ACC and LUSC, but favorable associations in KIRC, UCS and SCLC. The KIRC 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 KIRC as the clearest survival context for BRD2 RNA expression.
This table summarizes BRD2 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 5. The strongest signals are observed in HNSC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for BRD2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BRD2 shows lower tumor expression in THCA and KICH and higher tumor expression in HNSC, LIHC, STAD and CHOL. The HNSC box plot shows higher BRD2 RNA expression in tumor versus normal tissue (log2 FC = +0.844, t-test p < 0.001).
This table shows molecular features associated with BRD2 in patient tissues and cancer cell lines. In patient samples, BRD2 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, BRD2 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 LARGE_INTESTINE and BLOOD_Leukemia.
