Q-omics provides the consensus-scored TNKS1BP1 profile across patient tissues and cancer cell-line models. TNKS1BP1 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, TNKS1BP1 is differentially expressed in 7, with the highest sampling consensus in HNSC. Additionally, TNKS1BP1 protein abundance shows 22,579 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight UVM, and HNSC as cancer lineages where TNKS1BP1 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 TNKS1BP1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TNKS1BP1 survival associations across molecular data types. TNKS1BP1 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (9) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TNKS1BP1 RNA expression–survival associations across cancer types. High TNKS1BP1 expression shows unfavorable associations in UVM, LGG, KIRP and PAAD, but favorable associations in ESCA and SCLC. The UVM 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 UVM as the clearest survival context for TNKS1BP1 RNA expression.
This table summarizes TNKS1BP1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 7, while mass-spec protein shows differences in 5. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TNKS1BP1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TNKS1BP1 shows lower tumor expression in KICH and UCEC and higher tumor expression in HNSC, LIHC, CHOL and KIRC. The HNSC box plot shows higher TNKS1BP1 RNA expression in tumor versus normal tissue (log2 FC = +0.830, t-test p < 0.001).
This table shows molecular features associated with TNKS1BP1 in patient tissues and cancer cell lines. In patient samples, TNKS1BP1 shows the broadest associations at the RNA and protein expression levels, with HNSC recurring as the lineage with the largest associated feature set. In cancer cell lines, TNKS1BP1 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 LARGE_INTESTINE.
