protein kinase cAMP-dependent type I regulatory subunit alphaGenealiases: ACRDYS1 · ADOHR · CAR · CNC · CNC1 · PKR1
Q-omics provides the consensus-scored PRKAR1A profile across patient tissues and cancer cell-line models. PRKAR1A 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, PRKAR1A is differentially expressed in 11, with the highest sampling consensus in KICH. Additionally, PRKAR1A protein abundance shows 29,876 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRC, KICH, and PDAC as cancer lineages where PRKAR1A 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 PRKAR1A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRKAR1A survival associations across molecular data types. PRKAR1A RNA expression shows survival associations in the most cancer types (22), followed by mutation status (6) 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 PRKAR1A RNA expression–survival associations across cancer types. High PRKAR1A expression shows unfavorable associations in LGG, KIRP, CESC and HNSC, but favorable associations in KIRC and COAD. 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 PRKAR1A RNA expression.
This table summarizes PRKAR1A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 10. The strongest signals are observed in LUSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PRKAR1A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRKAR1A shows lower tumor expression in KICH, LUSC, UCEC, KIRC and LUAD and higher tumor expression in CHOL. The KICH box plot shows higher PRKAR1A RNA expression in normal versus tumor tissue (log2 FC = −1.007, t-test p < 0.001).
This table shows molecular features associated with PRKAR1A in patient tissues and cancer cell lines. In patient samples, PRKAR1A shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, PRKAR1A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in BONE and UPPER_AERODIGESTIVE_TRACT.
