Q-omics provides the consensus-scored TRRAP profile across patient tissues and cancer cell-line models. TRRAP expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, TRRAP is differentially expressed in 15, with the highest sampling consensus in KIRP. Additionally, TRRAP protein abundance shows 26,358 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight MESO, KIRP, and GBM as cancer lineages where TRRAP 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 TRRAP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TRRAP survival associations across molecular data types. TRRAP RNA expression shows survival associations in the most cancer types (24), followed by mutation status (14) 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 TRRAP RNA expression–survival associations across cancer types. High TRRAP expression shows unfavorable associations in MESO, LGG and KICH, but favorable associations in UCS, KIRC and THYM. The MESO Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify MESO as the clearest survival context for TRRAP RNA expression.
This table summarizes TRRAP 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 6. The strongest signals are observed in KIRP for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for TRRAP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TRRAP shows higher tumor expression in KIRP, HNSC, COAD, STAD, LUAD and BLCA. The KIRP box plot shows higher TRRAP RNA expression in tumor versus normal tissue (log2 FC = +0.929, t-test p < 0.001).
This table shows molecular features associated with TRRAP in patient tissues and cancer cell lines. In patient samples, TRRAP shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, TRRAP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LARGE_INTESTINE.
