Q-omics provides the consensus-scored TNKS profile across patient tissues and cancer cell-line models. TNKS expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, TNKS is differentially expressed in 10, with the highest sampling consensus in KIRP. Additionally, TNKS RNA expression shows 21,129 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight HNSC, KIRP, and ACC as cancer lineages where TNKS 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 TNKS — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TNKS survival associations across molecular data types. TNKS RNA expression shows survival associations in the most cancer types (27), followed by mutation status (8) 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 TNKS RNA expression–survival associations across cancer types. High TNKS expression shows unfavorable associations in ACC, MESO, KICH and STAD, but favorable associations in HNSC and KIRC. The HNSC 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 HNSC as the clearest survival context for TNKS RNA expression.
This table summarizes TNKS 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 4. The strongest signals are observed in KIRP for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for TNKS. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TNKS shows higher tumor expression in KIRP, LIHC, CHOL, STAD, LUSC and HNSC. The KIRP box plot shows higher TNKS RNA expression in tumor versus normal tissue (log2 FC = +0.885, t-test p < 0.001).
This table shows molecular features associated with TNKS in patient tissues and cancer cell lines. In patient samples, TNKS 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, TNKS RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in OVARY and UPPER_AERODIGESTIVE_TRACT.
