Q-omics provides the consensus-scored TNK2 profile across patient tissues and cancer cell-line models. TNK2 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, TNK2 is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, TNK2 RNA expression shows 18,678 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight UVM, HNSC, and ACC as cancer lineages where TNK2 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 TNK2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TNK2 survival associations across molecular data types. TNK2 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (10) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TNK2 RNA expression–survival associations across cancer types. High TNK2 expression shows unfavorable associations in COAD, but favorable associations in UVM, LGG, UCS, BLCA and HNSC. 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 TNK2 RNA expression.
This table summarizes TNK2 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 3. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for TNK2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TNK2 shows higher tumor expression in HNSC, KIRC, COAD, LIHC, LUSC and STAD. The HNSC box plot shows higher TNK2 RNA expression in tumor versus normal tissue (log2 FC = +1.146, t-test p < 0.001).
This table shows molecular features associated with TNK2 in patient tissues and cancer cell lines. In patient samples, TNK2 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, TNK2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and BLOOD_Lymphoma.
