Q-omics provides the consensus-scored TKT profile across patient tissues and cancer cell-line models. TKT expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, TKT is differentially expressed in 15, with the highest sampling consensus in KIRP. Additionally, TKT RNA expression shows 18,815 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight UVM, KIRP, and ACC as cancer lineages where TKT 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 TKT — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TKT survival associations across molecular data types. TKT RNA expression shows survival associations in the most cancer types (24), followed by mutation status (6) 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 TKT RNA expression–survival associations across cancer types. High TKT expression shows unfavorable associations in LIHC, ACC, MESO and SARC, but favorable associations in UVM and READ. The UVM 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 UVM as the clearest survival context for TKT RNA expression.
This table summarizes TKT tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRP for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for TKT. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TKT shows higher tumor expression in KIRP, COAD, LIHC, STAD, HNSC and LUAD. The KIRP box plot shows higher TKT RNA expression in tumor versus normal tissue (log2 FC = +2.149, t-test p < 0.001).
This table shows molecular features associated with TKT in patient tissues and cancer cell lines. In patient samples, TKT 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, TKT 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 UPPER_AERODIGESTIVE_TRACT and BREAST.
