Q-omics provides the consensus-scored SNRPN profile across patient tissues and cancer cell-line models. SNRPN expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, SNRPN is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, SNRPN RNA expression shows 18,369 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, and UVM as cancer lineages where SNRPN 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 SNRPN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SNRPN survival associations across molecular data types. SNRPN RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) 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 SNRPN RNA expression–survival associations across cancer types. High SNRPN expression shows unfavorable associations in ACC and DLBC, but favorable associations in KIRC, LGG, PAAD and SKCM. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for SNRPN RNA expression.
This table summarizes SNRPN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for SNRPN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SNRPN shows lower tumor expression in KIRC, THCA, KICH, LUSC, STAD and KIRP. The KIRC box plot shows higher SNRPN RNA expression in normal versus tumor tissue (log2 FC = −1.226, t-test p < 0.001).
This table shows molecular features associated with SNRPN in patient tissues and cancer cell lines. In patient samples, SNRPN shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, SNRPN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and SOFT_TISSUE.
