Q-omics provides the consensus-scored LURAP1L profile across patient tissues and cancer cell-line models. LURAP1L expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, LURAP1L is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, LURAP1L RNA expression shows 17,921 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, HNSC, and UVM as cancer lineages where LURAP1L 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 LURAP1L — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LURAP1L survival associations across molecular data types. LURAP1L RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) 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 LURAP1L RNA expression–survival associations across cancer types. High LURAP1L expression shows unfavorable associations in UVM and KIRP, but favorable associations in KIRC, BRCA, HNSC and OV. 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 LURAP1L RNA expression.
This table summarizes LURAP1L tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 4. The strongest signals are observed in HNSC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for LURAP1L. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LURAP1L shows lower tumor expression in LUAD, LUSC and UCEC and higher tumor expression in HNSC, THCA and KIRC. The HNSC box plot shows higher LURAP1L RNA expression in tumor versus normal tissue (log2 FC = +1.675, t-test p < 0.001).
This table shows molecular features associated with LURAP1L in patient tissues and cancer cell lines. In patient samples, LURAP1L 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, LURAP1L RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in BONE and STOMACH.
