Q-omics provides the consensus-scored PSMD13 profile across patient tissues and cancer cell-line models. PSMD13 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, PSMD13 is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, PSMD13 protein abundance shows 19,104 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight MESO, HNSC, and GBM as cancer lineages where PSMD13 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 PSMD13 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PSMD13 survival associations across molecular data types. PSMD13 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PSMD13 RNA expression–survival associations across cancer types. High PSMD13 expression shows unfavorable associations in MESO, ACC, KICH, LIHC, KIRC and HNSC. The MESO 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 MESO as the clearest survival context for PSMD13 RNA expression.
This table summarizes PSMD13 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 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PSMD13. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PSMD13 shows lower tumor expression in KICH and higher tumor expression in HNSC, KIRC, COAD, LIHC and STAD. The HNSC box plot shows higher PSMD13 RNA expression in tumor versus normal tissue (log2 FC = +0.705, t-test p < 0.001).
This table shows molecular features associated with PSMD13 in patient tissues and cancer cell lines. In patient samples, PSMD13 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, PSMD13 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 BLOOD_Leukemia.
