Q-omics provides the consensus-scored PSMA8 profile across patient tissues and cancer cell-line models. PSMA8 expression is associated with patient survival in 18 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, PSMA8 is differentially expressed in 7, with the highest sampling consensus in COAD. Additionally, PSMA8 RNA expression shows 10,338 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight HNSC, COAD, and THYM as cancer lineages where PSMA8 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 PSMA8 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PSMA8 survival associations across molecular data types. PSMA8 RNA expression shows survival associations in the most cancer types (18), followed by mutation status (1) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PSMA8 RNA expression–survival associations across cancer types. High PSMA8 expression shows unfavorable associations in UCS, but favorable associations in HNSC, CESC, BRCA, ESCA and SKCM. The HNSC 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 HNSC as the clearest survival context for PSMA8 RNA expression.
This table summarizes PSMA8 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 7, while mass-spec protein shows differences in 2. The strongest signals are observed in COAD for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for PSMA8. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PSMA8 shows lower tumor expression in COAD, THCA and LUSC and higher tumor expression in KIRC, CHOL and ESCA. The COAD box plot shows higher PSMA8 RNA expression in normal versus tumor tissue (log2 FC = −0.192, t-test p < 0.001).
This table shows molecular features associated with PSMA8 in patient tissues and cancer cell lines. In patient samples, PSMA8 shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, PSMA8 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Myeloma and LUNG_NSCLC_LUAD.
