Q-omics provides the consensus-scored TTBK2 profile across patient tissues and cancer cell-line models. TTBK2 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KICH. Among the 18 cancer types available for tumor–normal comparison, TTBK2 is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, TTBK2 RNA expression shows 22,284 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KICH, HNSC, and ACC as cancer lineages where TTBK2 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 TTBK2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TTBK2 survival associations across molecular data types. TTBK2 RNA expression shows survival associations in the most cancer types (26), 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 TTBK2 RNA expression–survival associations across cancer types. High TTBK2 expression shows unfavorable associations in KICH, UVM, ACC and HNSC, but favorable associations in SKCM and KIRC. The KICH Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .002). Together, the overview and detailed table identify KICH as the clearest survival context for TTBK2 RNA expression.
This table summarizes TTBK2 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 1. The strongest signals are observed in HNSC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for TTBK2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TTBK2 shows lower tumor expression in THCA, UCEC, BRCA and LUAD and higher tumor expression in HNSC and CHOL. The HNSC box plot shows higher TTBK2 RNA expression in tumor versus normal tissue (log2 FC = +0.877, t-test p < 0.001).
This table shows molecular features associated with TTBK2 in patient tissues and cancer cell lines. In patient samples, TTBK2 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, TTBK2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and BLOOD_Leukemia.
