Q-omics provides the consensus-scored PRELID3BP6 profile across patient tissues and cancer cell-line models. PRELID3BP6 expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, PRELID3BP6 is differentially expressed in 3, with the highest sampling consensus in KIRC. Additionally, PRELID3BP6 RNA expression shows 6,693 significant pathway-activity associations, with the highest sampling consensus in STAD. Together, these results highlight KIRP, KIRC, and STAD as cancer lineages where PRELID3BP6 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 PRELID3BP6 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRELID3BP6 survival associations across molecular data types. PRELID3BP6 RNA expression shows survival associations in the most cancer types (19). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PRELID3BP6 RNA expression–survival associations across cancer types. High PRELID3BP6 expression shows unfavorable associations in KIRP, THCA, LGG and LIHC, but favorable associations in HNSC and UCS. The KIRP 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 KIRP as the clearest survival context for PRELID3BP6 RNA expression.
This table summarizes PRELID3BP6 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 3. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for PRELID3BP6. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRELID3BP6 shows higher tumor expression in KIRC, STAD and LUAD. The KIRC box plot shows higher PRELID3BP6 RNA expression in tumor versus normal tissue (log2 FC = +0.046, t-test p = .002).
This table shows molecular features associated with PRELID3BP6 in patient tissues and cancer cell lines. In patient samples, PRELID3BP6 shows the broadest associations at the RNA and protein expression levels, with STAD recurring as the lineage with the largest associated feature set.
