Q-omics provides the consensus-scored SNRNP25 profile across patient tissues and cancer cell-line models. SNRNP25 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, SNRNP25 is differentially expressed in 14, with the highest sampling consensus in THCA. Additionally, SNRNP25 RNA expression shows 18,380 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight UVM, THCA, and THYM as cancer lineages where SNRNP25 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 SNRNP25 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SNRNP25 survival associations across molecular data types. SNRNP25 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (2) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SNRNP25 RNA expression–survival associations across cancer types. High SNRNP25 expression shows unfavorable associations in UVM, ACC, UCS, SKCM, LAML and ESCA. The UVM 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 UVM as the clearest survival context for SNRNP25 RNA expression.
This table summarizes SNRNP25 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 1. The strongest signals are observed in THCA for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for SNRNP25. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SNRNP25 shows lower tumor expression in THCA and higher tumor expression in LIHC, LUAD, BRCA, HNSC and KIRP. The THCA box plot shows higher SNRNP25 RNA expression in normal versus tumor tissue (log2 FC = −0.931, t-test p < 0.001).
This table shows molecular features associated with SNRNP25 in patient tissues and cancer cell lines. In patient samples, SNRNP25 shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, SNRNP25 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 BREAST and BLOOD_Lymphoma.
