Q-omics provides the consensus-scored GSTA3 profile across patient tissues and cancer cell-line models. GSTA3 expression is associated with patient survival in 11 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, GSTA3 is differentially expressed in 11, with the highest sampling consensus in LUAD. Additionally, GSTA3 RNA expression shows 8,832 significant protein co-abundance associations, with the highest sampling consensus in UCEC. Together, these results highlight UVM, LUAD, and UCEC as cancer lineages where GSTA3 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 GSTA3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GSTA3 survival associations across molecular data types. GSTA3 RNA expression shows survival associations in the most cancer types (11), followed by mutation status (4) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible GSTA3 RNA expression–survival associations across cancer types. High GSTA3 expression shows unfavorable associations in CHOL, BLCA, READ and THCA, but favorable associations in UVM and LUAD. The UVM 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 UVM as the clearest survival context for GSTA3 RNA expression.
This table summarizes GSTA3 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 2. The strongest signals are observed in LUAD for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for GSTA3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GSTA3 shows lower tumor expression in LUAD, LUSC, KIRP and STAD and higher tumor expression in KICH and BRCA. The LUAD box plot shows higher GSTA3 RNA expression in normal versus tumor tissue (log2 FC = −1.883, t-test p < 0.001).
This table shows molecular features associated with GSTA3 in patient tissues and cancer cell lines. In patient samples, GSTA3 shows the broadest associations at the RNA and protein expression levels, with UCEC recurring as the lineage with the largest associated feature set. In cancer cell lines, GSTA3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and BREAST.
