Q-omics provides the consensus-scored PSMG2 profile across patient tissues and cancer cell-line models. PSMG2 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, PSMG2 is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, PSMG2 protein abundance shows 21,593 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight ACC, KIRC, and GBM as cancer lineages where PSMG2 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 PSMG2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PSMG2 survival associations across molecular data types. PSMG2 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (2) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PSMG2 RNA expression–survival associations across cancer types. High PSMG2 expression shows unfavorable associations in ACC, LIHC, LUAD and UVM, but favorable associations in KIRC and OV. 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 PSMG2 RNA expression.
This table summarizes PSMG2 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 6. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for PSMG2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PSMG2 shows lower tumor expression in KICH and higher tumor expression in KIRC, LIHC, HNSC, BLCA and CHOL. The KIRC box plot shows higher PSMG2 RNA expression in tumor versus normal tissue (log2 FC = +0.424, t-test p < 0.001).
This table shows molecular features associated with PSMG2 in patient tissues and cancer cell lines. In patient samples, PSMG2 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, PSMG2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and UPPER_AERODIGESTIVE_TRACT.
