Q-omics provides the consensus-scored THRA profile across patient tissues and cancer cell-line models. THRA expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, THRA is differentially expressed in 14, with the highest sampling consensus in BLCA. Additionally, THRA protein abundance shows 32,436 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRC, BLCA, and LUAD as cancer lineages where THRA 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 THRA — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes THRA survival associations across molecular data types. THRA RNA expression shows survival associations in the most cancer types (26), followed by mutation status (7) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible THRA RNA expression–survival associations across cancer types. High THRA expression shows unfavorable associations in BLCA, but favorable associations in KIRC, LGG, READ, UVM and ACC. 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 THRA RNA expression.
This table summarizes THRA tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 10. The strongest signals are observed in BLCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for THRA. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. THRA shows lower tumor expression in BLCA, LUAD, THCA, KICH and UCEC and higher tumor expression in LIHC. The BLCA box plot shows higher THRA RNA expression in normal versus tumor tissue (log2 FC = −2.297, t-test p < 0.001).
This table shows molecular features associated with THRA in patient tissues and cancer cell lines. In patient samples, THRA 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, THRA RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and CNS.
