Q-omics provides the consensus-scored SLN profile across patient tissues and cancer cell-line models. SLN 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, SLN is differentially expressed in 8, with the highest sampling consensus in KIRC. Additionally, SLN RNA expression shows 12,781 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight KIRC, and HNSC as cancer lineages where SLN 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 SLN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SLN survival associations across molecular data types. SLN RNA expression shows survival associations in the most cancer types (24), followed by mutation status (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SLN RNA expression–survival associations across cancer types. High SLN expression shows unfavorable associations in KIRC, THCA, CESC, HNSC, LIHC and UCEC. The KIRC 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 KIRC as the clearest survival context for SLN RNA expression.
This table summarizes SLN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for SLN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SLN shows lower tumor expression in HNSC, LUSC and KICH and higher tumor expression in KIRC, BRCA and COAD. The KIRC box plot shows higher SLN RNA expression in tumor versus normal tissue (log2 FC = +1.026, t-test p < 0.001).
This table shows molecular features associated with SLN in patient tissues and cancer cell lines. In patient samples, SLN shows the broadest associations at the RNA and protein expression levels, with HNSC recurring as the lineage with the largest associated feature set. In cancer cell lines, SLN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in OVARY and UPPER_AERODIGESTIVE_TRACT.
