Q-omics provides the consensus-scored TNS1 profile across patient tissues and cancer cell-line models. TNS1 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, TNS1 is differentially expressed in 17, with the highest sampling consensus in BLCA. Additionally, TNS1 protein abundance shows 34,909 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRC, BLCA, and LUAD as cancer lineages where TNS1 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 TNS1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TNS1 survival associations across molecular data types. TNS1 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (9) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TNS1 RNA expression–survival associations across cancer types. High TNS1 expression shows unfavorable associations in BLCA, OV and ACC, but favorable associations in KIRC, HNSC 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 TNS1 RNA expression.
This table summarizes TNS1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 17, while mass-spec protein shows differences in 6. The strongest signals are observed in BLCA for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for TNS1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TNS1 shows lower tumor expression in BLCA, THCA, KICH, LUSC, LUAD and COAD. The BLCA box plot shows higher TNS1 RNA expression in normal versus tumor tissue (log2 FC = −5.230, t-test p < 0.001).
This table shows molecular features associated with TNS1 in patient tissues and cancer cell lines. In patient samples, TNS1 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, TNS1 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 SOFT_TISSUE and LARGE_INTESTINE.
