Q-omics provides the consensus-scored PLPPR3 profile across patient tissues and cancer cell-line models. PLPPR3 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PLPPR3 is differentially expressed in 8, with the highest sampling consensus in LUSC. Additionally, PLPPR3 RNA expression shows 14,756 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KIRC, LUSC, and TGCT as cancer lineages where PLPPR3 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 PLPPR3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PLPPR3 survival associations across molecular data types. PLPPR3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (6) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PLPPR3 RNA expression–survival associations across cancer types. High PLPPR3 expression shows unfavorable associations in KIRC, OV, ACC, CESC and COAD, but favorable associations in 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 PLPPR3 RNA expression.
This table summarizes PLPPR3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8. The strongest signals are observed in LUSC for RNA.
This table ranks reproducible tumor–normal expression differences for PLPPR3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PLPPR3 shows lower tumor expression in LUSC and LUAD and higher tumor expression in THCA, BRCA, READ and STAD. The LUSC box plot shows higher PLPPR3 RNA expression in normal versus tumor tissue (log2 FC = −1.602, t-test p < 0.001).
This table shows molecular features associated with PLPPR3 in patient tissues and cancer cell lines. In patient samples, PLPPR3 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, PLPPR3 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 BLOOD_Leukemia and SOFT_TISSUE.
