Q-omics provides the consensus-scored TLK1 profile across patient tissues and cancer cell-line models. TLK1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, TLK1 is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, TLK1 RNA expression shows 21,579 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight ACC, HNSC, and UVM as cancer lineages where TLK1 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 TLK1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TLK1 survival associations across molecular data types. TLK1 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (5) 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 TLK1 RNA expression–survival associations across cancer types. High TLK1 expression shows unfavorable associations in ACC, UVM, LGG and HNSC, but favorable associations in KIRC and SKCM. The ACC 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 ACC as the clearest survival context for TLK1 RNA expression.
This table summarizes TLK1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 5. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for TLK1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TLK1 shows lower tumor expression in KIRC and higher tumor expression in HNSC, LIHC, LUAD, LUSC and CHOL. The HNSC box plot shows higher TLK1 RNA expression in tumor versus normal tissue (log2 FC = +1.062, t-test p < 0.001).
This table shows molecular features associated with TLK1 in patient tissues and cancer cell lines. In patient samples, TLK1 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, TLK1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BLOOD_Leukemia.
