Q-omics provides the consensus-scored PLPBP profile across patient tissues and cancer cell-line models. PLPBP expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PLPBP is differentially expressed in 14, with the highest sampling consensus in THCA. Additionally, PLPBP RNA expression shows 18,385 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, THCA, and ACC as cancer lineages where PLPBP 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 PLPBP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PLPBP survival associations across molecular data types. PLPBP RNA expression shows survival associations in the most cancer types (26), followed by mutation status (1) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PLPBP RNA expression–survival associations across cancer types. High PLPBP expression shows unfavorable associations in LGG, but favorable associations in KIRC, LUSC, HNSC, MESO and BLCA. 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 PLPBP RNA expression.
This table summarizes PLPBP 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 6. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PLPBP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PLPBP shows lower tumor expression in THCA, KICH, KIRC, COAD, LUAD and KIRP. The THCA box plot shows higher PLPBP RNA expression in normal versus tumor tissue (log2 FC = −0.321, t-test p < 0.001).
This table shows molecular features associated with PLPBP in patient tissues and cancer cell lines. In patient samples, PLPBP shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, PLPBP 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_Myeloma and BLOOD_Leukemia.
