Q-omics provides the consensus-scored PSMA3 profile across patient tissues and cancer cell-line models. PSMA3 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, PSMA3 is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, PSMA3 protein abundance shows 28,851 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight UVM, HNSC, and PDAC as cancer lineages where PSMA3 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 PSMA3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PSMA3 survival associations across molecular data types. PSMA3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (3) 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 PSMA3 RNA expression–survival associations across cancer types. High PSMA3 expression shows unfavorable associations in UVM, KICH, HNSC, ACC, LUAD and LIHC. The UVM 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 UVM as the clearest survival context for PSMA3 RNA expression.
This table summarizes PSMA3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 9. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PSMA3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PSMA3 shows higher tumor expression in HNSC, STAD, LIHC, BLCA, COAD and UCEC. The HNSC box plot shows higher PSMA3 RNA expression in tumor versus normal tissue (log2 FC = +0.719, t-test p < 0.001).
This table shows molecular features associated with PSMA3 in patient tissues and cancer cell lines. In patient samples, PSMA3 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, PSMA3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in SKIN and CNS.
