Q-omics provides the consensus-scored TBCC profile across patient tissues and cancer cell-line models. TBCC expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, TBCC is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, TBCC protein abundance shows 26,670 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight MESO, KIRC, and GBM as cancer lineages where TBCC 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 TBCC — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TBCC survival associations across molecular data types. TBCC RNA expression shows survival associations in the most cancer types (26), followed by mutation status (6) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TBCC RNA expression–survival associations across cancer types. High TBCC expression shows unfavorable associations in LIHC, LAML and KICH, but favorable associations in MESO, LUAD and KIRC. The MESO Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .001). Together, the overview and detailed table identify MESO as the clearest survival context for TBCC RNA expression.
This table summarizes TBCC 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 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TBCC. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TBCC shows lower tumor expression in THCA and KICH and higher tumor expression in KIRC, HNSC, LIHC and KIRP. The KIRC box plot shows higher TBCC RNA expression in tumor versus normal tissue (log2 FC = +0.514, t-test p < 0.001).
This table shows molecular features associated with TBCC in patient tissues and cancer cell lines. In patient samples, TBCC 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, TBCC RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and SOFT_TISSUE.
