Q-omics provides the consensus-scored TRIP13 profile across patient tissues and cancer cell-line models. TRIP13 expression is associated with patient survival in 30 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, TRIP13 is differentially expressed in 16, with the highest sampling consensus in KIRC. Additionally, TRIP13 RNA expression shows 26,126 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, KIRC, and GBM as cancer lineages where TRIP13 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 TRIP13 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TRIP13 survival associations across molecular data types. TRIP13 RNA expression shows survival associations in the most cancer types (30), followed by mutation status (6) 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 TRIP13 RNA expression–survival associations across cancer types. High TRIP13 expression shows unfavorable associations in KIRP, ACC, MESO, KICH, KIRC and LIHC. The KIRP 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 KIRP as the clearest survival context for TRIP13 RNA expression.
This table summarizes TRIP13 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TRIP13. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TRIP13 shows higher tumor expression in KIRC, LUAD, BLCA, HNSC, COAD and KIRP. The KIRC box plot shows higher TRIP13 RNA expression in tumor versus normal tissue (log2 FC = +1.440, t-test p < 0.001).
This table shows molecular features associated with TRIP13 in patient tissues and cancer cell lines. In patient samples, TRIP13 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, TRIP13 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in STOMACH and BLOOD_Leukemia.
