Q-omics provides the consensus-scored STN1 profile across patient tissues and cancer cell-line models. STN1 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, STN1 is differentially expressed in 11, with the highest sampling consensus in LIHC. Additionally, STN1 RNA expression shows 19,281 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, LIHC, and ACC as cancer lineages where STN1 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 STN1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes STN1 survival associations across molecular data types. STN1 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (7) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible STN1 RNA expression–survival associations across cancer types. High STN1 expression shows unfavorable associations in PAAD and ACC, but favorable associations in KIRC, THCA, CHOL and UCS. 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 STN1 RNA expression.
This table summarizes STN1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 6. The strongest signals are observed in LIHC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for STN1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. STN1 shows lower tumor expression in HNSC, LUSC and KICH and higher tumor expression in LIHC, CHOL and THCA. The LIHC box plot shows higher STN1 RNA expression in tumor versus normal tissue (log2 FC = +1.179, t-test p < 0.001).
This table shows molecular features associated with STN1 in patient tissues and cancer cell lines. In patient samples, STN1 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, STN1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and SOFT_TISSUE.
