Q-omics provides the consensus-scored PKIA profile across patient tissues and cancer cell-line models. PKIA expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, PKIA is differentially expressed in 14, with the highest sampling consensus in THCA. Additionally, PKIA protein abundance shows 24,879 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight UVM, THCA, and GBM as cancer lineages where PKIA 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 PKIA — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PKIA survival associations across molecular data types. PKIA RNA expression shows survival associations in the most cancer types (24), followed by mutation status (4) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PKIA RNA expression–survival associations across cancer types. High PKIA expression shows unfavorable associations in UVM and UCEC, but favorable associations in SKCM, UCS, BRCA and LGG. The UVM 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 UVM as the clearest survival context for PKIA RNA expression.
This table summarizes PKIA 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 5. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PKIA. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PKIA shows lower tumor expression in THCA, KIRC, LUAD, HNSC and UCEC and higher tumor expression in KICH. The THCA box plot shows higher PKIA RNA expression in normal versus tumor tissue (log2 FC = −2.595, t-test p < 0.001).
This table shows molecular features associated with PKIA in patient tissues and cancer cell lines. In patient samples, PKIA 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, PKIA RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BLOOD_Leukemia.
