Q-omics provides the consensus-scored PRELID2 profile across patient tissues and cancer cell-line models. PRELID2 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PRELID2 is differentially expressed in 16, with the highest sampling consensus in KIRC. Additionally, PRELID2 RNA expression shows 19,113 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, and UVM as cancer lineages where PRELID2 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 PRELID2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRELID2 survival associations across molecular data types. PRELID2 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PRELID2 RNA expression–survival associations across cancer types. High PRELID2 expression shows unfavorable associations in UCEC, KICH, HNSC, LGG and LIHC, but favorable associations in KIRC. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for PRELID2 RNA expression.
This table summarizes PRELID2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for PRELID2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRELID2 shows lower tumor expression in KICH and COAD and higher tumor expression in KIRC, HNSC, LUAD and KIRP. The KIRC box plot shows higher PRELID2 RNA expression in tumor versus normal tissue (log2 FC = +1.536, t-test p < 0.001).
This table shows molecular features associated with PRELID2 in patient tissues and cancer cell lines. In patient samples, PRELID2 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, PRELID2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in OESOPHAGUS and BLOOD_Lymphoma.
