Q-omics provides the consensus-scored TPR profile across patient tissues and cancer cell-line models. TPR expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, TPR is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, TPR protein abundance shows 31,301 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight ACC, HNSC, and GBM as cancer lineages where TPR 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 TPR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TPR survival associations across molecular data types. TPR RNA expression shows survival associations in the most cancer types (25), followed by mutation status (12) 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 TPR RNA expression–survival associations across cancer types. High TPR expression shows unfavorable associations in ACC, KIRP, UVM, KICH and LIHC, but favorable associations in KIRC. The ACC 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 ACC as the clearest survival context for TPR RNA expression.
This table summarizes TPR 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 8. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for TPR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TPR shows higher tumor expression in HNSC, LIHC, BLCA, KIRP, KIRC and BRCA. The HNSC box plot shows higher TPR RNA expression in tumor versus normal tissue (log2 FC = +0.849, t-test p < 0.001).
This table shows molecular features associated with TPR in patient tissues and cancer cell lines. In patient samples, TPR shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, TPR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in KIDNEY and BLOOD_Leukemia.
