Q-omics provides the consensus-scored PRKACA profile across patient tissues and cancer cell-line models. PRKACA expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KICH. Among the 18 cancer types available for tumor–normal comparison, PRKACA is differentially expressed in 11, with the highest sampling consensus in COAD. Additionally, PRKACA protein abundance shows 30,651 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KICH, COAD, and LSCC as cancer lineages where PRKACA 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 PRKACA — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRKACA survival associations across molecular data types. PRKACA RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) and mass-spec protein abundance (14). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PRKACA RNA expression–survival associations across cancer types. High PRKACA expression shows unfavorable associations in KICH, LGG, MESO, BLCA and ACC, but favorable associations in PAAD. The KICH 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 KICH as the clearest survival context for PRKACA RNA expression.
This table summarizes PRKACA 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 12. The strongest signals are observed in COAD for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for PRKACA. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRKACA shows lower tumor expression in COAD, LUAD, READ and BLCA and higher tumor expression in LIHC and ESCA. The COAD box plot shows higher PRKACA RNA expression in normal versus tumor tissue (log2 FC = −0.468, t-test p < 0.001).
This table shows molecular features associated with PRKACA in patient tissues and cancer cell lines. In patient samples, PRKACA shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, PRKACA 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 BLOOD_Leukemia and LARGE_INTESTINE.
