Q-omics provides the consensus-scored PLAUR profile across patient tissues and cancer cell-line models. PLAUR expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PLAUR is differentially expressed in 13, with the highest sampling consensus in THCA. Additionally, PLAUR protein abundance shows 26,497 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, THCA, and GBM as cancer lineages where PLAUR 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 PLAUR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PLAUR survival associations across molecular data types. PLAUR RNA expression shows survival associations in the most cancer types (27), followed by mutation status (4) 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 PLAUR RNA expression–survival associations across cancer types. High PLAUR expression shows unfavorable associations in KIRC, ACC, MESO, OV, LUAD and LGG. The KIRC 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 KIRC as the clearest survival context for PLAUR RNA expression.
This table summarizes PLAUR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 6. The strongest signals are observed in THCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for PLAUR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PLAUR shows higher tumor expression in THCA, HNSC, KIRC, COAD, STAD and KIRP. The THCA box plot shows higher PLAUR RNA expression in tumor versus normal tissue (log2 FC = +3.338, t-test p < 0.001).
This table shows molecular features associated with PLAUR in patient tissues and cancer cell lines. In patient samples, PLAUR shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, PLAUR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in SKIN and SOFT_TISSUE.
