Q-omics provides the consensus-scored TPT1 profile across patient tissues and cancer cell-line models. TPT1 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in UCEC. Among the 18 cancer types available for tumor–normal comparison, TPT1 is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, TPT1 protein abundance shows 22,501 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight UCEC, KIRC, and PDAC as cancer lineages where TPT1 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 TPT1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TPT1 survival associations across molecular data types. TPT1 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (4) 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 TPT1 RNA expression–survival associations across cancer types. High TPT1 expression shows unfavorable associations in OV, BLCA and ACC, but favorable associations in UCEC, MESO and BRCA. The UCEC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .001). Together, the overview and detailed table identify UCEC as the clearest survival context for TPT1 RNA expression.
This table summarizes TPT1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TPT1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TPT1 shows lower tumor expression in BLCA, LUSC, HNSC, KICH and UCEC and higher tumor expression in KIRC. The KIRC box plot shows higher TPT1 RNA expression in tumor versus normal tissue (log2 FC = +0.790, t-test p < 0.001).
This table shows molecular features associated with TPT1 in patient tissues and cancer cell lines. In patient samples, TPT1 shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, TPT1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Myeloma, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BLOOD_Leukemia.
