transmembrane phosphatase with tensin homologyGenealiases: CT44 · PTEN2 · TPTE1
Q-omics provides the consensus-scored TPTE profile across patient tissues and cancer cell-line models. TPTE expression is associated with patient survival in 14 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, TPTE is differentially expressed in 5, with the highest sampling consensus in KIRC. Additionally, TPTE RNA expression shows 9,055 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight MESO, KIRC, and TGCT as cancer lineages where TPTE 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 TPTE — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TPTE survival associations across molecular data types. TPTE RNA expression shows survival associations in the most cancer types (14), followed by mutation status (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TPTE RNA expression–survival associations across cancer types. High TPTE expression shows unfavorable associations in MESO, KIRC, KIRP, COAD and BRCA, but favorable associations in LUAD. The MESO 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 MESO as the clearest survival context for TPTE RNA expression.
This table summarizes TPTE tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 5. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for TPTE. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TPTE shows lower tumor expression in KIRC and higher tumor expression in BRCA, LIHC, LUAD and UCEC. The KIRC box plot shows higher TPTE RNA expression in normal versus tumor tissue (log2 FC = −0.018, t-test p = .001).
This table shows molecular features associated with TPTE in patient tissues and cancer cell lines. In patient samples, TPTE shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, TPTE RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and LARGE_INTESTINE.
