protein tyrosine phosphatase receptor type UGenealiases: FMI · PCP-2 · PTP · PTP-J · PTP-PI · PTP-RO
Q-omics provides the consensus-scored PTPRU profile across patient tissues and cancer cell-line models. PTPRU expression is associated with patient survival in 17 of 34 cancer types, with the highest sampling consensus in OV. Among the 18 cancer types available for tumor–normal comparison, PTPRU is differentially expressed in 12, with the highest sampling consensus in COAD. Additionally, PTPRU protein abundance shows 29,338 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight OV, COAD, and LSCC as cancer lineages where PTPRU 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 PTPRU — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PTPRU survival associations across molecular data types. PTPRU RNA expression shows survival associations in the most cancer types (17), followed by mutation status (10) and mass-spec protein abundance (11). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PTPRU RNA expression–survival associations across cancer types. High PTPRU expression shows unfavorable associations in OV, PAAD, LUSC, COAD and READ, but favorable associations in ACC. The OV Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .003). Together, the overview and detailed table identify OV as the clearest survival context for PTPRU RNA expression.
This table summarizes PTPRU tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 11. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PTPRU. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PTPRU shows lower tumor expression in KICH and LUSC and higher tumor expression in COAD, KIRC, THCA and CHOL. The COAD box plot shows higher PTPRU RNA expression in tumor versus normal tissue (log2 FC = +1.209, t-test p < 0.001).
This table shows molecular features associated with PTPRU in patient tissues and cancer cell lines. In patient samples, PTPRU shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, PTPRU 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 BLOOD_Myeloma and BLOOD_Leukemia.
