Q-omics provides the consensus-scored PREX1 profile across patient tissues and cancer cell-line models. PREX1 expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, PREX1 is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, PREX1 protein abundance shows 23,633 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight UVM, KIRC, and LSCC as cancer lineages where PREX1 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 PREX1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PREX1 survival associations across molecular data types. PREX1 RNA expression shows survival associations in the most cancer types (28), followed by mutation status (9) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PREX1 RNA expression–survival associations across cancer types. High PREX1 expression shows unfavorable associations in UVM and LGG, but favorable associations in KIRC, HNSC, BRCA and UCEC. The UVM 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 UVM as the clearest survival context for PREX1 RNA expression.
This table summarizes PREX1 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 5. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PREX1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PREX1 shows lower tumor expression in LUAD and LUSC and higher tumor expression in KIRC, STAD, LIHC and BRCA. The KIRC box plot shows higher PREX1 RNA expression in tumor versus normal tissue (log2 FC = +1.786, t-test p < 0.001).
This table shows molecular features associated with PREX1 in patient tissues and cancer cell lines. In patient samples, PREX1 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, PREX1 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 BREAST and BONE.
