protein kinase Y-linked (pseudogene)Genealiases: PRKXP3 · PRKYP
Q-omics provides the consensus-scored PRKY profile across patient tissues and cancer cell-line models. PRKY expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, PRKY is differentially expressed in 7, with the highest sampling consensus in KIRC. Additionally, PRKY RNA expression shows 7,851 significant protein co-abundance associations, with the highest sampling consensus in BRCA. Together, these results highlight BLCA, KIRC, and BRCA as cancer lineages where PRKY 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 PRKY — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRKY survival associations across molecular data types. PRKY RNA expression shows survival associations in the most cancer types (22). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PRKY RNA expression–survival associations across cancer types. High PRKY expression shows unfavorable associations in DLBC and LIHC, but favorable associations in BLCA, HNSC, UVM and READ. The BLCA 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 BLCA as the clearest survival context for PRKY RNA expression.
This table summarizes PRKY tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 7. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for PRKY. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRKY shows lower tumor expression in THCA, PRAD, KICH and KIRP and higher tumor expression in KIRC and CHOL. The KIRC box plot shows higher PRKY RNA expression in tumor versus normal tissue (log2 FC = +0.556, t-test p < 0.001).
This table shows molecular features associated with PRKY in patient tissues and cancer cell lines. In patient samples, PRKY shows the broadest associations at the RNA and protein expression levels, with BRCA recurring as the lineage with the largest associated feature set. In cancer cell lines, PRKY RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in SKIN.
