Q-omics provides the consensus-scored BFAR profile across patient tissues and cancer cell-line models. BFAR 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, BFAR is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, BFAR RNA expression shows 20,294 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight ACC, and HNSC as cancer lineages where BFAR 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 BFAR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BFAR survival associations across molecular data types. BFAR RNA expression shows survival associations in the most cancer types (26), followed by mutation status (6) 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 BFAR RNA expression–survival associations across cancer types. High BFAR expression shows unfavorable associations in ACC, MESO, BLCA, SCLC and PAAD, but favorable associations in KIRC. 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 BFAR RNA expression.
This table summarizes BFAR 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 3. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for BFAR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BFAR shows higher tumor expression in HNSC, KIRC, KIRP, LIHC, COAD and STAD. The HNSC box plot shows higher BFAR RNA expression in tumor versus normal tissue (log2 FC = +1.301, t-test p < 0.001).
This table shows molecular features associated with BFAR in patient tissues and cancer cell lines. In patient samples, BFAR 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, BFAR 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 LIVER and UPPER_AERODIGESTIVE_TRACT.
