Q-omics provides the consensus-scored PTP4A2 profile across patient tissues and cancer cell-line models. PTP4A2 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, PTP4A2 is differentially expressed in 12, with the highest sampling consensus in THCA. Additionally, PTP4A2 RNA expression shows 19,882 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRP, THCA, and ACC as cancer lineages where PTP4A2 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 PTP4A2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PTP4A2 survival associations across molecular data types. PTP4A2 RNA expression shows survival associations in the most cancer types (27), followed by mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PTP4A2 RNA expression–survival associations across cancer types. High PTP4A2 expression shows unfavorable associations in KIRP, KICH, LIHC, CESC and LGG, but favorable associations in BLCA. The KIRP 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 KIRP as the clearest survival context for PTP4A2 RNA expression.
This table summarizes PTP4A2 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 6. The strongest signals are observed in THCA for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for PTP4A2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PTP4A2 shows lower tumor expression in THCA, KICH and LUSC and higher tumor expression in STAD, HNSC and BRCA. The THCA box plot shows higher PTP4A2 RNA expression in normal versus tumor tissue (log2 FC = −0.655, t-test p < 0.001).
This table shows molecular features associated with PTP4A2 in patient tissues and cancer cell lines. In patient samples, PTP4A2 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, PTP4A2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and BREAST.
