Q-omics provides the consensus-scored LDLR profile across patient tissues and cancer cell-line models. LDLR expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, LDLR is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, LDLR RNA expression shows 19,538 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRP, KIRC, and ACC as cancer lineages where LDLR 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 LDLR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LDLR survival associations across molecular data types. LDLR RNA expression shows survival associations in the most cancer types (24), followed by mutation status (11) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LDLR RNA expression–survival associations across cancer types. High LDLR expression shows unfavorable associations in KIRP, BLCA, MESO, UVM and ACC, but favorable associations in SKCM. 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 LDLR RNA expression.
This table summarizes LDLR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for LDLR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LDLR shows lower tumor expression in KIRC, KIRP, LUAD and LUSC and higher tumor expression in COAD and THCA. The KIRC box plot shows higher LDLR RNA expression in normal versus tumor tissue (log2 FC = −1.491, t-test p < 0.001).
This table shows molecular features associated with LDLR in patient tissues and cancer cell lines. In patient samples, LDLR shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, LDLR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and LARGE_INTESTINE.
