Q-omics provides the consensus-scored THBD profile across patient tissues and cancer cell-line models. THBD expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, THBD is differentially expressed in 12, with the highest sampling consensus in LUAD. Additionally, THBD RNA expression shows 19,755 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight UVM, LUAD, and GBM as cancer lineages where THBD 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 THBD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes THBD survival associations across molecular data types. THBD RNA expression shows survival associations in the most cancer types (27), followed by mutation status (2) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible THBD RNA expression–survival associations across cancer types. High THBD expression shows unfavorable associations in UVM, MESO, THCA and LGG, but favorable associations in KIRC and UCS. The UVM 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 UVM as the clearest survival context for THBD RNA expression.
This table summarizes THBD 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 3. The strongest signals are observed in LUAD for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for THBD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. THBD shows lower tumor expression in LUAD, THCA, KICH, UCEC, LUSC and BRCA. The LUAD box plot shows higher THBD RNA expression in normal versus tumor tissue (log2 FC = −2.375, t-test p < 0.001).
This table shows molecular features associated with THBD in patient tissues and cancer cell lines. In patient samples, THBD 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, THBD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUSC, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and BONE.
