Q-omics provides the consensus-scored TXN profile across patient tissues and cancer cell-line models. TXN expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, TXN is differentially expressed in 15, with the highest sampling consensus in LIHC. Additionally, TXN RNA expression shows 18,454 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight LUAD, LIHC, and THYM as cancer lineages where TXN 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 TXN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TXN survival associations across molecular data types. TXN RNA expression shows survival associations in the most cancer types (25), followed by mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TXN RNA expression–survival associations across cancer types. High TXN expression shows unfavorable associations in LUAD, ACC, LIHC, HNSC and UCS, but favorable associations in UCEC. The LUAD 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 LUAD as the clearest survival context for TXN RNA expression.
This table summarizes TXN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 1. The strongest signals are observed in LIHC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for TXN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TXN shows higher tumor expression in LIHC, KIRC, LUSC, LUAD, KIRP and BLCA. The LIHC box plot shows higher TXN RNA expression in tumor versus normal tissue (log2 FC = +1.709, t-test p < 0.001).
This table shows molecular features associated with TXN in patient tissues and cancer cell lines. In patient samples, TXN shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, TXN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and CNS.
