Q-omics provides the consensus-scored BTD profile across patient tissues and cancer cell-line models. BTD expression is associated with patient survival in 17 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, BTD is differentially expressed in 16, with the highest sampling consensus in COAD. Additionally, BTD protein abundance shows 25,076 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRC, COAD, and PDAC as cancer lineages where BTD 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 BTD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BTD survival associations across molecular data types. BTD RNA expression shows survival associations in the most cancer types (17), followed by mutation status (6) 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 BTD RNA expression–survival associations across cancer types. High BTD expression shows unfavorable associations in LUSC, but favorable associations in KIRC, BRCA, READ, PRAD and LIHC. 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 BTD RNA expression.
This table summarizes BTD tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 6. The strongest signals are observed in COAD for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for BTD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BTD shows lower tumor expression in COAD, KIRC, THCA, UCEC, KICH and LUSC. The COAD box plot shows higher BTD RNA expression in normal versus tumor tissue (log2 FC = −0.952, t-test p < 0.001).
This table shows molecular features associated with BTD in patient tissues and cancer cell lines. In patient samples, BTD shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, BTD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BLOOD_Lymphoma.
