Q-omics provides the consensus-scored TBP profile across patient tissues and cancer cell-line models. TBP expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in OV. Among the 18 cancer types available for tumor–normal comparison, TBP is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, TBP RNA expression shows 20,225 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight OV, HNSC, and ACC as cancer lineages where TBP 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 TBP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TBP survival associations across molecular data types. TBP RNA expression shows survival associations in the most cancer types (24), followed by mutation status (4) 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 TBP RNA expression–survival associations across cancer types. High TBP expression shows unfavorable associations in OV, LIHC, MESO, KIRC and BRCA, but favorable associations in READ. The OV Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .002). Together, the overview and detailed table identify OV as the clearest survival context for TBP RNA expression.
This table summarizes TBP tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 4. The strongest signals are observed in HNSC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for TBP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TBP shows lower tumor expression in KICH and THCA and higher tumor expression in HNSC, COAD, LIHC and CHOL. The HNSC box plot shows higher TBP RNA expression in tumor versus normal tissue (log2 FC = +0.940, t-test p < 0.001).
This table shows molecular features associated with TBP in patient tissues and cancer cell lines. In patient samples, TBP 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, TBP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and BLOOD_Leukemia.
