Q-omics provides the consensus-scored UTP25 profile across patient tissues and cancer cell-line models. UTP25 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, UTP25 is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, UTP25 protein abundance shows 31,708 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRP, HNSC, and LSCC as cancer lineages where UTP25 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 UTP25 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes UTP25 survival associations across molecular data types. UTP25 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (5) 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 UTP25 RNA expression–survival associations across cancer types. High UTP25 expression shows unfavorable associations in KIRP, PAAD, CESC, LIHC and ACC, but favorable associations in KIRC. 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 UTP25 RNA expression.
This table summarizes UTP25 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 UTP25. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. UTP25 shows higher tumor expression in HNSC, COAD, KIRC, LIHC, LUAD and STAD. The HNSC box plot shows higher UTP25 RNA expression in tumor versus normal tissue (log2 FC = +0.925, t-test p < 0.001).
This table shows molecular features associated with UTP25 in patient tissues and cancer cell lines. In patient samples, UTP25 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, UTP25 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and LARGE_INTESTINE.
