Q-omics provides the consensus-scored PLAA profile across patient tissues and cancer cell-line models. PLAA expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PLAA is differentially expressed in 15, with the highest sampling consensus in THCA. Additionally, PLAA RNA expression shows 19,273 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, THCA, and UVM as cancer lineages where PLAA 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 PLAA — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PLAA survival associations across molecular data types. PLAA RNA expression shows survival associations in the most cancer types (20), followed by mutation status (4) and 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 PLAA RNA expression–survival associations across cancer types. High PLAA expression shows unfavorable associations in ACC, UVM, PAAD, LIHC and CESC, but favorable associations in KIRC. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for PLAA RNA expression.
This table summarizes PLAA tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 7. The strongest signals are observed in THCA for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for PLAA. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PLAA shows lower tumor expression in THCA and higher tumor expression in LIHC, COAD, HNSC, BRCA and STAD. The THCA box plot shows higher PLAA RNA expression in normal versus tumor tissue (log2 FC = −0.287, t-test p < 0.001).
This table shows molecular features associated with PLAA in patient tissues and cancer cell lines. In patient samples, PLAA 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, PLAA 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 LUNG_NSCLC_LUAD and BLOOD_Lymphoma.