Q-omics provides the consensus-scored BPTF profile across patient tissues and cancer cell-line models. BPTF expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, BPTF is differentially expressed in 13, with the highest sampling consensus in THCA. Additionally, BPTF protein abundance shows 29,340 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, THCA, and GBM as cancer lineages where BPTF 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 BPTF — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BPTF survival associations across molecular data types. BPTF RNA expression shows survival associations in the most cancer types (26), followed by mutation status (5) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible BPTF RNA expression–survival associations across cancer types. High BPTF expression shows unfavorable associations in LIHC, LUSC, CESC and BLCA, but favorable associations in KIRC and READ. 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 BPTF RNA expression.
This table summarizes BPTF tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 4. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for BPTF. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BPTF shows lower tumor expression in THCA and KICH and higher tumor expression in HNSC, BLCA, LIHC and CHOL. The THCA box plot shows higher BPTF RNA expression in normal versus tumor tissue (log2 FC = −0.686, t-test p < 0.001).
This table shows molecular features associated with BPTF in patient tissues and cancer cell lines. In patient samples, BPTF shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, BPTF RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LARGE_INTESTINE.
