Q-omics provides the consensus-scored SNTG1 profile across patient tissues and cancer cell-line models. SNTG1 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, SNTG1 is differentially expressed in 9, with the highest sampling consensus in KIRC. Additionally, SNTG1 RNA expression shows 8,110 significant gene co-expression associations, with the highest sampling consensus in BLCA. Together, these results highlight KIRC, and BLCA as cancer lineages where SNTG1 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 SNTG1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SNTG1 survival associations across molecular data types. SNTG1 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (5) 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 SNTG1 RNA expression–survival associations across cancer types. High SNTG1 expression shows unfavorable associations in KIRC, ACC, KICH, CESC and THCA, but favorable associations in LGG. 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 SNTG1 RNA expression.
This table summarizes SNTG1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for SNTG1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SNTG1 shows lower tumor expression in KIRC, KIRP, COAD and KICH and higher tumor expression in LIHC and PAAD. The KIRC box plot shows higher SNTG1 RNA expression in normal versus tumor tissue (log2 FC = −0.303, t-test p < 0.001).
This table shows molecular features associated with SNTG1 in patient tissues and cancer cell lines. In patient samples, SNTG1 shows the broadest associations at the RNA and protein expression levels, with BLCA recurring as the lineage with the largest associated feature set. In cancer cell lines, SNTG1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and OVARY.
