Q-omics provides the consensus-scored LEPR profile across patient tissues and cancer cell-line models. LEPR expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, LEPR is differentially expressed in 16, with the highest sampling consensus in KICH. Additionally, LEPR RNA expression shows 18,641 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, KICH, and UVM as cancer lineages where LEPR 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 LEPR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LEPR survival associations across molecular data types. LEPR RNA expression shows survival associations in the most cancer types (22), followed by mutation status (2) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LEPR RNA expression–survival associations across cancer types. High LEPR expression shows unfavorable associations in CESC, KICH and OV, but favorable associations in KIRC, SKCM and ACC. 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 LEPR RNA expression.
This table summarizes LEPR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 7. The strongest signals are observed in KICH for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for LEPR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LEPR shows lower tumor expression in KICH, LUAD, THCA, COAD, LUSC and BLCA. The KICH box plot shows higher LEPR RNA expression in normal versus tumor tissue (log2 FC = −2.843, t-test p < 0.001).
This table shows molecular features associated with LEPR in patient tissues and cancer cell lines. In patient samples, LEPR 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, LEPR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and BLOOD_Lymphoma.
