Q-omics provides the consensus-scored PRR3 profile across patient tissues and cancer cell-line models. PRR3 expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, PRR3 is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, PRR3 RNA expression shows 20,423 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRP, KIRC, and ACC as cancer lineages where PRR3 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 PRR3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRR3 survival associations across molecular data types. PRR3 RNA expression shows survival associations in the most cancer types (28), followed by mutation status (2) 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 PRR3 RNA expression–survival associations across cancer types. High PRR3 expression shows unfavorable associations in KIRP, ACC, KICH, UCEC and LIHC, but favorable associations in OV. The KIRP Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .002). Together, the overview and detailed table identify KIRP as the clearest survival context for PRR3 RNA expression.
This table summarizes PRR3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 4. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for PRR3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRR3 shows higher tumor expression in KIRC, HNSC, LIHC, LUAD, COAD and KIRP. The KIRC box plot shows higher PRR3 RNA expression in tumor versus normal tissue (log2 FC = +0.668, t-test p < 0.001).
This table shows molecular features associated with PRR3 in patient tissues and cancer cell lines. In patient samples, PRR3 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, PRR3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BONE.
