Q-omics provides the consensus-scored PVR profile across patient tissues and cancer cell-line models. PVR expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, PVR is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, PVR RNA expression shows 19,072 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRP, HNSC, and ACC as cancer lineages where PVR 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 PVR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PVR survival associations across molecular data types. PVR RNA expression shows survival associations in the most cancer types (21), followed by mutation status (7) 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 PVR RNA expression–survival associations across cancer types. High PVR expression shows unfavorable associations in KIRP, HNSC, BLCA, MESO, BRCA and CESC. The KIRP 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 KIRP as the clearest survival context for PVR RNA expression.
This table summarizes PVR 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 8. The strongest signals are observed in HNSC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for PVR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PVR shows higher tumor expression in HNSC, COAD, KIRP, STAD, LIHC and KIRC. The HNSC box plot shows higher PVR RNA expression in tumor versus normal tissue (log2 FC = +1.661, t-test p < 0.001).
This table shows molecular features associated with PVR in patient tissues and cancer cell lines. In patient samples, PVR 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, PVR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in BONE and BREAST.
