Q-omics provides the consensus-scored TTK profile across patient tissues and cancer cell-line models. TTK expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, TTK is differentially expressed in 17, with the highest sampling consensus in HNSC. Additionally, TTK protein abundance shows 35,840 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRP, HNSC, and LSCC as cancer lineages where TTK 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 TTK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TTK survival associations across molecular data types. TTK RNA expression shows survival associations in the most cancer types (27), followed by mutation status (7) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TTK RNA expression–survival associations across cancer types. High TTK expression shows unfavorable associations in KIRP, ACC, MESO, LIHC, KICH and KIRC. The KIRP 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 KIRP as the clearest survival context for TTK RNA expression.
This table summarizes TTK tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 17, while mass-spec protein shows differences in 11. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for TTK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TTK shows higher tumor expression in HNSC, KIRC, BLCA, LUAD, KIRP and STAD. The HNSC box plot shows higher TTK RNA expression in tumor versus normal tissue (log2 FC = +1.835, t-test p < 0.001).
This table shows molecular features associated with TTK in patient tissues and cancer cell lines. In patient samples, TTK shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, TTK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in OVARY and BLOOD_Leukemia.
