Q-omics provides the consensus-scored PRKAG1 profile across patient tissues and cancer cell-line models. PRKAG1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in LIHC. Among the 18 cancer types available for tumor–normal comparison, PRKAG1 is differentially expressed in 12, with the highest sampling consensus in LIHC. Additionally, PRKAG1 protein abundance shows 20,147 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight LIHC, and GBM as cancer lineages where PRKAG1 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 PRKAG1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRKAG1 survival associations across molecular data types. PRKAG1 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PRKAG1 RNA expression–survival associations across cancer types. High PRKAG1 expression shows unfavorable associations in LIHC, HNSC, UVM, MESO and LAML, but favorable associations in KIRC. The LIHC 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 LIHC as the clearest survival context for PRKAG1 RNA expression.
This table summarizes PRKAG1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 5. The strongest signals are observed in LIHC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for PRKAG1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRKAG1 shows higher tumor expression in LIHC, HNSC, COAD, BLCA, BRCA and CHOL. The LIHC box plot shows higher PRKAG1 RNA expression in tumor versus normal tissue (log2 FC = +1.076, t-test p < 0.001).
This table shows molecular features associated with PRKAG1 in patient tissues and cancer cell lines. In patient samples, PRKAG1 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, PRKAG1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and UPPER_AERODIGESTIVE_TRACT.
