Q-omics provides the consensus-scored GGA1 profile across patient tissues and cancer cell-line models. GGA1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, GGA1 is differentially expressed in 9, with the highest sampling consensus in LIHC. Additionally, GGA1 protein abundance shows 23,462 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight ACC, LIHC, and GBM as cancer lineages where GGA1 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 GGA1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GGA1 survival associations across molecular data types. GGA1 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (8) and mass-spec protein abundance (11). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible GGA1 RNA expression–survival associations across cancer types. High GGA1 expression shows unfavorable associations in ACC, LIHC, KIRC and LAML, but favorable associations in ESCA and KIRP. The ACC 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 ACC as the clearest survival context for GGA1 RNA expression.
This table summarizes GGA1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 11. The strongest signals are observed in LIHC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for GGA1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GGA1 shows higher tumor expression in LIHC, STAD, CHOL, KIRP, PRAD and ESCA. The LIHC box plot shows higher GGA1 RNA expression in tumor versus normal tissue (log2 FC = +1.359, t-test p < 0.001).
This table shows molecular features associated with GGA1 in patient tissues and cancer cell lines. In patient samples, GGA1 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, GGA1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and LARGE_INTESTINE.
