Q-omics provides the consensus-scored PPIH profile across patient tissues and cancer cell-line models. PPIH expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PPIH is differentially expressed in 16, with the highest sampling consensus in HNSC. Additionally, PPIH protein abundance shows 22,765 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, HNSC, and GBM as cancer lineages where PPIH 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 PPIH — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PPIH survival associations across molecular data types. PPIH RNA expression shows survival associations in the most cancer types (24), followed by mutation status (1) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PPIH RNA expression–survival associations across cancer types. High PPIH expression shows unfavorable associations in KIRC, ACC, KIRP, LIHC, KICH and 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 PPIH RNA expression.
This table summarizes PPIH tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PPIH. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PPIH shows higher tumor expression in HNSC, KIRC, COAD, LIHC, BLCA and LUAD. The HNSC box plot shows higher PPIH RNA expression in tumor versus normal tissue (log2 FC = +0.921, t-test p < 0.001).
This table shows molecular features associated with PPIH in patient tissues and cancer cell lines. In patient samples, PPIH shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, PPIH RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and BLOOD_Lymphoma.
