Q-omics provides the consensus-scored PPID profile across patient tissues and cancer cell-line models. PPID expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, PPID is differentially expressed in 11, with the highest sampling consensus in THCA. Additionally, PPID RNA expression shows 19,175 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight HNSC, THCA, and ACC as cancer lineages where PPID 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 PPID — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PPID survival associations across molecular data types. PPID RNA expression shows survival associations in the most cancer types (28), followed by mutation status (4) 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 PPID RNA expression–survival associations across cancer types. High PPID expression shows unfavorable associations in HNSC, CESC, LUAD, MESO and LGG, but favorable associations in KIRC. The HNSC 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 HNSC as the clearest survival context for PPID RNA expression.
This table summarizes PPID 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 6. The strongest signals are observed in THCA for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for PPID. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PPID shows lower tumor expression in THCA and KIRC and higher tumor expression in HNSC, LUSC, STAD and LUAD. The THCA box plot shows higher PPID RNA expression in normal versus tumor tissue (log2 FC = −0.582, t-test p < 0.001).
This table shows molecular features associated with PPID in patient tissues and cancer cell lines. In patient samples, PPID 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, PPID 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 BONE and UPPER_AERODIGESTIVE_TRACT.
