Q-omics provides the consensus-scored TTPA profile across patient tissues and cancer cell-line models. TTPA expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in UCEC. Among the 18 cancer types available for tumor–normal comparison, TTPA is differentially expressed in 9, with the highest sampling consensus in KIRC. Additionally, TTPA RNA expression shows 17,389 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight UCEC, KIRC, and UVM as cancer lineages where TTPA 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 TTPA — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TTPA survival associations across molecular data types. TTPA RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TTPA RNA expression–survival associations across cancer types. High TTPA expression shows unfavorable associations in UCEC, UVM and LUAD, but favorable associations in LGG, SCLC and LIHC. The UCEC 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 UCEC as the clearest survival context for TTPA RNA expression.
This table summarizes TTPA tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 3. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for TTPA. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TTPA shows lower tumor expression in KIRC, KIRP, LUAD, KICH, LUSC and BRCA. The KIRC box plot shows higher TTPA RNA expression in normal versus tumor tissue (log2 FC = −1.054, t-test p < 0.001).
This table shows molecular features associated with TTPA in patient tissues and cancer cell lines. In patient samples, TTPA 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, TTPA RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in LIVER and SKIN.
