Q-omics provides the consensus-scored TOR3A profile across patient tissues and cancer cell-line models. TOR3A expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, TOR3A is differentially expressed in 16, with the highest sampling consensus in BLCA. Additionally, TOR3A RNA expression shows 19,053 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight UVM, BLCA, and ACC as cancer lineages where TOR3A 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 TOR3A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TOR3A survival associations across molecular data types. TOR3A RNA expression shows survival associations in the most cancer types (23), followed by mutation status (3) and 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 TOR3A RNA expression–survival associations across cancer types. High TOR3A expression shows unfavorable associations in UVM, KIRC, ACC, KIRP and LGG, but favorable associations in DLBC. The UVM 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 UVM as the clearest survival context for TOR3A RNA expression.
This table summarizes TOR3A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 4. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for TOR3A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TOR3A shows higher tumor expression in BLCA, KIRC, HNSC, LIHC, STAD and KIRP. The BLCA box plot shows higher TOR3A RNA expression in tumor versus normal tissue (log2 FC = +1.190, t-test p < 0.001).
This table shows molecular features associated with TOR3A in patient tissues and cancer cell lines. In patient samples, TOR3A 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, TOR3A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and SOFT_TISSUE.
