Q-omics provides the consensus-scored TRIAP1 profile across patient tissues and cancer cell-line models. TRIAP1 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, TRIAP1 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, TRIAP1 RNA expression shows 18,146 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight MESO, KIRC, and UVM as cancer lineages where TRIAP1 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 TRIAP1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TRIAP1 survival associations across molecular data types. TRIAP1 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (3) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TRIAP1 RNA expression–survival associations across cancer types. High TRIAP1 expression shows unfavorable associations in MESO, LUAD, LIHC, KIRP, LGG and KICH. The MESO 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 MESO as the clearest survival context for TRIAP1 RNA expression.
This table summarizes TRIAP1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TRIAP1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TRIAP1 shows higher tumor expression in KIRC, KIRP, BLCA, LIHC, STAD and COAD. The KIRC box plot shows higher TRIAP1 RNA expression in tumor versus normal tissue (log2 FC = +0.618, t-test p < 0.001).
This table shows molecular features associated with TRIAP1 in patient tissues and cancer cell lines. In patient samples, TRIAP1 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, TRIAP1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and UPPER_AERODIGESTIVE_TRACT.
