Q-omics provides the consensus-scored PREX2 profile across patient tissues and cancer cell-line models. PREX2 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, PREX2 is differentially expressed in 14, with the highest sampling consensus in LUAD. Additionally, PREX2 RNA expression shows 19,071 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRP, LUAD, and UVM as cancer lineages where PREX2 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 PREX2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PREX2 survival associations across molecular data types. PREX2 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (5) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PREX2 RNA expression–survival associations across cancer types. High PREX2 expression shows unfavorable associations in KIRP, UVM, BLCA and LUSC, but favorable associations in HNSC and UCS. 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 PREX2 RNA expression.
This table summarizes PREX2 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 4. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for PREX2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PREX2 shows lower tumor expression in LUAD, THCA, KICH, LUSC and COAD and higher tumor expression in KIRC. The LUAD box plot shows higher PREX2 RNA expression in normal versus tumor tissue (log2 FC = −2.098, t-test p < 0.001).
This table shows molecular features associated with PREX2 in patient tissues and cancer cell lines. In patient samples, PREX2 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, PREX2 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 BLOOD_Leukemia and LARGE_INTESTINE.
