Q-omics provides the consensus-scored PZP profile across patient tissues and cancer cell-line models. PZP expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, PZP is differentially expressed in 11, with the highest sampling consensus in LIHC. Additionally, PZP RNA expression shows 18,898 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight SKCM, LIHC, and LSCC as cancer lineages where PZP 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 PZP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PZP survival associations across molecular data types. PZP RNA expression shows survival associations in the most cancer types (26), followed by mutation status (8) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PZP RNA expression–survival associations across cancer types. High PZP expression shows unfavorable associations in KIRP and LAML, but favorable associations in SKCM, UCEC, HNSC and LIHC. The SKCM 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 SKCM as the clearest survival context for PZP RNA expression.
This table summarizes PZP 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 7. The strongest signals are observed in LIHC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for PZP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PZP shows lower tumor expression in LIHC, LUSC, LUAD, KICH and BRCA and higher tumor expression in KIRC. The LIHC box plot shows higher PZP RNA expression in normal versus tumor tissue (log2 FC = −4.558, t-test p < 0.001).
This table shows molecular features associated with PZP in patient tissues and cancer cell lines. In patient samples, PZP 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, PZP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in OESOPHAGUS and LARGE_INTESTINE.
