Q-omics provides the consensus-scored SNAPIN profile across patient tissues and cancer cell-line models. SNAPIN expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, SNAPIN is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, SNAPIN protein abundance shows 19,507 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight UVM, KIRC, and GBM as cancer lineages where SNAPIN 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 SNAPIN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SNAPIN survival associations across molecular data types. SNAPIN RNA expression shows survival associations in the most cancer types (21), followed by mutation status (2) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SNAPIN RNA expression–survival associations across cancer types. High SNAPIN expression shows unfavorable associations in UVM, ACC, LIHC, KICH, LAML and LGG. 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 SNAPIN RNA expression.
This table summarizes SNAPIN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, 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 SNAPIN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SNAPIN shows lower tumor expression in KICH and higher tumor expression in KIRC, HNSC, LIHC, BLCA and LUAD. The KIRC box plot shows higher SNAPIN RNA expression in tumor versus normal tissue (log2 FC = +0.424, t-test p < 0.001).
This table shows molecular features associated with SNAPIN in patient tissues and cancer cell lines. In patient samples, SNAPIN 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, SNAPIN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and UPPER_AERODIGESTIVE_TRACT.
