Q-omics provides the consensus-scored SNRK profile across patient tissues and cancer cell-line models. SNRK expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, SNRK is differentially expressed in 10, with the highest sampling consensus in LUAD. Additionally, SNRK protein abundance shows 22,700 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, LUAD, and LSCC as cancer lineages where SNRK 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 SNRK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SNRK survival associations across molecular data types. SNRK RNA expression shows survival associations in the most cancer types (24), followed by mutation status (3) 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 SNRK RNA expression–survival associations across cancer types. High SNRK expression shows unfavorable associations in LUSC, but favorable associations in KIRC, HNSC, BRCA, UCS and COAD. 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 SNRK RNA expression.
This table summarizes SNRK tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 4. The strongest signals are observed in LUSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for SNRK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SNRK shows lower tumor expression in LUAD, LUSC, BLCA, THCA, KICH and COAD. The LUAD box plot shows higher SNRK RNA expression in normal versus tumor tissue (log2 FC = −1.634, t-test p < 0.001).
This table shows molecular features associated with SNRK in patient tissues and cancer cell lines. In patient samples, SNRK 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, SNRK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in SKIN and UPPER_AERODIGESTIVE_TRACT.
