Q-omics provides the consensus-scored LDLRAD3 profile across patient tissues and cancer cell-line models. LDLRAD3 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, LDLRAD3 is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, LDLRAD3 RNA expression shows 19,439 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight LUAD, KIRC, and THYM as cancer lineages where LDLRAD3 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 LDLRAD3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LDLRAD3 survival associations across molecular data types. LDLRAD3 RNA expression shows survival associations in the most cancer types (24), 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 LDLRAD3 RNA expression–survival associations across cancer types. High LDLRAD3 expression shows unfavorable associations in LUAD, UVM, KIRP, BLCA and MESO, but favorable associations in BRCA. The LUAD 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 LUAD as the clearest survival context for LDLRAD3 RNA expression.
This table summarizes LDLRAD3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for LDLRAD3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LDLRAD3 shows higher tumor expression in KIRC, KIRP, COAD, THCA, LUSC and HNSC. The KIRC box plot shows higher LDLRAD3 RNA expression in tumor versus normal tissue (log2 FC = +1.485, t-test p < 0.001).
This table shows molecular features associated with LDLRAD3 in patient tissues and cancer cell lines. In patient samples, LDLRAD3 shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, LDLRAD3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in SKIN and SOFT_TISSUE.
