Q-omics provides the consensus-scored PRELID3BP8 profile across patient tissues and cancer cell-line models. PRELID3BP8 expression is associated with patient survival in 9 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PRELID3BP8 is differentially expressed in 2, with the highest sampling consensus in HNSC. Additionally, PRELID3BP8 RNA expression shows 6,629 significant gene co-expression associations, with the highest sampling consensus in COAD. Together, these results highlight KIRC, HNSC, and COAD as cancer lineages where PRELID3BP8 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 PRELID3BP8 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRELID3BP8 survival associations across molecular data types. PRELID3BP8 RNA expression shows survival associations in the most cancer types (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PRELID3BP8 RNA expression–survival associations across cancer types. High PRELID3BP8 expression shows unfavorable associations in KIRC, KICH, THCA and GBM, but favorable associations in ESCA and PRAD. The KIRC 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 KIRC as the clearest survival context for PRELID3BP8 RNA expression.
This table summarizes PRELID3BP8 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 HNSC for RNA.
This table ranks reproducible tumor–normal expression differences for PRELID3BP8. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRELID3BP8 shows lower tumor expression in HNSC and higher tumor expression in KIRC. The HNSC box plot shows higher PRELID3BP8 RNA expression in normal versus tumor tissue (log2 FC = −0.021, t-test p = .042).
This table shows molecular features associated with PRELID3BP8 in patient tissues and cancer cell lines. In patient samples, PRELID3BP8 shows the broadest associations at the RNA and protein expression levels, with COAD recurring as the lineage with the largest associated feature set.
