Q-omics provides the consensus-scored TRIP6 profile across patient tissues and cancer cell-line models. TRIP6 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in COAD. Among the 18 cancer types available for tumor–normal comparison, TRIP6 is differentially expressed in 13, with the highest sampling consensus in COAD. Additionally, TRIP6 protein abundance shows 24,221 significant protein co-abundance associations, with the highest sampling consensus in UCEC. Together, these results highlight COAD, and UCEC as cancer lineages where TRIP6 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 TRIP6 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TRIP6 survival associations across molecular data types. TRIP6 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TRIP6 RNA expression–survival associations across cancer types. High TRIP6 expression shows unfavorable associations in COAD, LGG, LAML, OV and PAAD, but favorable associations in KIRP. The COAD 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 COAD as the clearest survival context for TRIP6 RNA expression.
This table summarizes TRIP6 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 8. The strongest signals are observed in COAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TRIP6. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TRIP6 shows lower tumor expression in KICH and UCEC and higher tumor expression in COAD, KIRP, HNSC and CHOL. The COAD box plot shows higher TRIP6 RNA expression in tumor versus normal tissue (log2 FC = +1.747, t-test p < 0.001).
This table shows molecular features associated with TRIP6 in patient tissues and cancer cell lines. In patient samples, TRIP6 shows the broadest associations at the RNA and protein expression levels, with UCEC recurring as the lineage with the largest associated feature set. In cancer cell lines, TRIP6 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 OESOPHAGUS and CNS.
