Q-omics provides the consensus-scored BCL7A profile across patient tissues and cancer cell-line models. BCL7A expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, BCL7A is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, BCL7A protein abundance shows 21,605 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight ACC, HNSC, and LSCC as cancer lineages where BCL7A 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 BCL7A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BCL7A survival associations across molecular data types. BCL7A RNA expression shows survival associations in the most cancer types (26), followed by mutation status (5) 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 BCL7A RNA expression–survival associations across cancer types. High BCL7A expression shows unfavorable associations in ACC, MESO, LIHC and HNSC, but favorable associations in KIRC and UCS. 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 BCL7A RNA expression.
This table summarizes BCL7A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 7. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for BCL7A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BCL7A shows lower tumor expression in KIRC and higher tumor expression in HNSC, COAD, LIHC, STAD and LUSC. The HNSC box plot shows higher BCL7A RNA expression in tumor versus normal tissue (log2 FC = +1.171, t-test p < 0.001).
This table shows molecular features associated with BCL7A in patient tissues and cancer cell lines. In patient samples, BCL7A 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, BCL7A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BLOOD_Leukemia.
