Q-omics provides the consensus-scored TCHH profile across patient tissues and cancer cell-line models. TCHH expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, TCHH is differentially expressed in 10, with the highest sampling consensus in COAD. Additionally, TCHH RNA expression shows 15,013 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight UVM, and COAD as cancer lineages where TCHH 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 TCHH — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TCHH survival associations across molecular data types. TCHH RNA expression shows survival associations in the most cancer types (25), followed by mutation status (8) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TCHH RNA expression–survival associations across cancer types. High TCHH expression shows unfavorable associations in UVM, BLCA, OV and COAD, but favorable associations in UCS and LGG. 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 TCHH RNA expression.
This table summarizes TCHH tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 1. The strongest signals are observed in COAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TCHH. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TCHH shows lower tumor expression in LIHC and LUAD and higher tumor expression in COAD, BRCA, THCA and KIRP. The COAD box plot shows higher TCHH RNA expression in tumor versus normal tissue (log2 FC = +0.181, t-test p < 0.001).
This table shows molecular features associated with TCHH in patient tissues and cancer cell lines. In patient samples, TCHH shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, TCHH RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in BONE and LARGE_INTESTINE.
