Q-omics provides the consensus-scored PRAMEF33 profile across patient tissues and cancer cell-line models. PRAMEF33 expression is associated with patient survival in 11 of 34 cancer types, with the highest sampling consensus in BRCA. Among the 18 cancer types available for tumor–normal comparison, PRAMEF33 is differentially expressed in 2, with the highest sampling consensus in CHOL. Additionally, PRAMEF33 RNA expression shows 7,682 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight BRCA, CHOL, and TGCT as cancer lineages where PRAMEF33 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 PRAMEF33 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRAMEF33 survival associations across molecular data types. PRAMEF33 RNA expression shows survival associations in the most cancer types (11), followed by mutation status (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PRAMEF33 RNA expression–survival associations across cancer types. High PRAMEF33 expression shows unfavorable associations in BRCA, SKCM, LUSC, STAD and CESC, but favorable associations in LIHC. The BRCA 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 BRCA as the clearest survival context for PRAMEF33 RNA expression.
This table summarizes PRAMEF33 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 2. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for PRAMEF33. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRAMEF33 shows lower tumor expression in CHOL and higher tumor expression in KIRC. The CHOL box plot shows higher PRAMEF33 RNA expression in normal versus tumor tissue (log2 FC = −0.507, t-test p = .013).
This table shows molecular features associated with PRAMEF33 in patient tissues and cancer cell lines. In patient samples, PRAMEF33 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, PRAMEF33 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 LUNG_SCLC.
