Q-omics provides the consensus-scored PRKX profile across patient tissues and cancer cell-line models. PRKX expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PRKX is differentially expressed in 13, with the highest sampling consensus in THCA. Additionally, PRKX RNA expression shows 19,714 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, THCA, and UVM as cancer lineages where PRKX 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 PRKX — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRKX survival associations across molecular data types. PRKX RNA expression shows survival associations in the most cancer types (22), followed by mutation status (3) 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 PRKX RNA expression–survival associations across cancer types. High PRKX expression shows unfavorable associations in ACC, UVM and MESO, but favorable associations in KIRC, SCLC and LUSC. The KIRC 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 KIRC as the clearest survival context for PRKX RNA expression.
This table summarizes PRKX 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 3. The strongest signals are observed in THCA for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for PRKX. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRKX shows lower tumor expression in THCA, KICH and KIRC and higher tumor expression in BLCA, STAD and COAD. The THCA box plot shows higher PRKX RNA expression in normal versus tumor tissue (log2 FC = −2.115, t-test p < 0.001).
This table shows molecular features associated with PRKX in patient tissues and cancer cell lines. In patient samples, PRKX shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, PRKX RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and SOFT_TISSUE.
